@article{Arezki2022b,

title = {Surface charge influences protein corona, cell uptake and biological effects of carbon dots},

author = {Y Arezki and F Delalande and C Schaeffer-Reiss and S Cianferani and M Rapp and L Lebeau and F Pons and C Ronzani},

url = {https://www.ncbi.nlm.nih.gov/pubmed/36168840},

doi = {10.1039/d2nr03611h},

issn = {2040-3372 (Electronic) 2040-3364 (Linking)},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Nanoscale},

abstract = {Carbon dots are emerging nanoparticles (NPs) with tremendous applications, especially in the biomedical field. Herein is reported the first quantitative proteomic analysis of the protein corona formed on CDs with different surface charge properties. Four CDs were synthesized from citric acid and various amine group-containing passivation reagents, resulting in cationic NPs with increasing zeta (zeta)-potential and density of positive charges. After CD contact with serum, we show that protein corona identity is influenced by CD surface charge properties, which in turn impacts CD uptake and viability loss in macrophages. In particular, CDs with high zeta-potential (+30 mV) and charge density (2 mumol mg(-1)) are the most highly internalized, and their cell uptake is strongly correlated with a corona enriched in vitronectin, fibulin, fetuin, adiponectin and alpha-glycoprotein. On the contrary, CDs with a lower zeta-potential (+11 mV) and charge density (0.01 mumol mg(-1)) are poorly internalized, while having a corona with a very different protein signature characterized by a high abundance of apolipoproteins (APOA1, APOB and APOC), albumin and hemoglobin. These data illustrate how corona characterization may contribute to a better understanding of CD cellular fate and biological effects, and provide useful information for the development of CDs for biomedical applications.},

note = {Type: Journal Article},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {SMYD3 Impedes Small Cell Lung Cancer Sensitivity to Alkylation Damage through RNF113A Methylation-Phosphorylation Cross-talk},

author = {Valentina Lukinović and Simone Hausmann and Gael S Roth and Clement Oyeniran and Tanveer Ahmad and Ning Tsao and Joshua R Brickner and Alexandre G Casanova and Florent Chuffart and Ana Morales Benitez and Jessica Vayr and Rebecca Rodell and Marianne Tardif and Pascal W T C Jansen and Yohann Couté and Michiel Vermeulen and Pierre Hainaut and Pawel K Mazur and Nima Mosammaparast and Nicolas Reynoird},

doi = {10.1158/2159-8290.CD-21-0205},

issn = {2159-8290},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Cancer Discovery},

volume = {12},

issue = {9},

pages = {2158-2179},

abstract = {Small cell lung cancer (SCLC) is the most fatal form of lung cancer, with dismal survival, limited therapeutic options, and rapid development of chemoresistance. We identified the lysine methyltransferase SMYD3 as a major regulator of SCLC sensitivity to alkylation-based chemotherapy. RNF113A methylation by SMYD3 impairs its interaction with the phosphatase PP4, controlling its phosphorylation levels. This cross-talk between posttranslational modifications acts as a key switch in promoting and maintaining RNF113A E3 ligase activity, essential for its role in alkylation damage response. In turn, SMYD3 inhibition restores SCLC vulnerability to alkylating chemotherapy. Our study sheds light on a novel role of SMYD3 in cancer, uncovering this enzyme as a mediator of alkylation damage sensitivity and providing a rationale for small-molecule SMYD3 inhibition to improve responses to established chemotherapy. SIGNIFICANCE: SCLC rapidly becomes resistant to conventional chemotherapy, leaving patients with no alternative treatment options. Our data demonstrate that SMYD3 upregulation and RNF113A methylation in SCLC are key mechanisms that control the alkylation damage response. Notably, SMYD3 inhibition sensitizes cells to alkylating agents and promotes sustained SCLC response to chemotherapy. This article is highlighted in the In This Issue feature, p. 2007.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Villalta2022b,

title = {The giant mimivirus 1.2 Mb genome is elegantly organized into a 30-nm diameter helical protein shield},

author = {Alejandro Villalta and Alain Schmitt and Leandro F Estrozi and Emmanuelle R J Quemin and Jean-Marie Alempic and Audrey Lartigue and Vojtěch Pražák and Lucid Belmudes and Daven Vasishtan and Agathe M G Colmant and Flora A Honoré and Yohann Couté and Kay Grünewald and Chantal Abergel},

doi = {10.7554/eLife.77607},

issn = {2050-084X},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {eLife},

volume = {11},

pages = {e77607},

abstract = {Mimivirus is the prototype of the Mimiviridae family of giant dsDNA viruses. Little is known about the organization of the 1.2 Mb genome inside the membrane-limited nucleoid filling the textasciitilde0.5 µm icosahedral capsids. Cryo-electron microscopy, cryo-electron tomography, and proteomics revealed that it is encased into a textasciitilde30-nm diameter helical protein shell surprisingly composed of two GMC-type oxidoreductases, which also form the glycosylated fibrils decorating the capsid. The genome is arranged in 5- or 6-start left-handed super-helices, with each DNA-strand lining the central channel. This luminal channel of the nucleoprotein fiber is wide enough to accommodate oxidative stress proteins and RNA polymerase subunits identified by proteomics. Such elegant supramolecular organization would represent a remarkable evolutionary strategy for packaging and protecting the genome, in a state ready for immediate transcription upon unwinding in the host cytoplasm. The parsimonious use of the same protein in two unrelated substructures of the virion is unexpected for a giant virus with thousand genes at its disposal.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Barnault2022b,

title = {Hepatic inflammation elicits production of proinflammatory netrin-1 through exclusive activation of translation},

author = {Romain Barnault and Claire Verzeroli and Carole Fournier and Maud Michelet and Anna Rita Redavid and Ievgeniia Chicherova and Marie-Laure Plissonnier and Annie Adrait and Olga Khomich and Fleur Chapus and Mathieu Richaud and Maëva Hervieu and Veronika Reiterer and Federica Grazia Centonze and Julie Lucifora and Birke Bartosch and Michel Rivoire and Hesso Farhan and Yohann Couté and Valbona Mirakaj and Thomas Decaens and Patrick Mehlen and Benjamin Gibert and Fabien Zoulim and Romain Parent},

doi = {10.1002/hep.32446},

issn = {1527-3350},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Hepatology (Baltimore, Md.)},

volume = {76},

issue = {5},

pages = {1345-1359},

abstract = {BACKGROUND AND AIMS: Netrin-1 displays protumoral properties, though the pathological contexts and processes involved in its induction remain understudied. The liver is a major model of inflammation-associated cancer development, leading to HCC. APPROACH AND RESULTS: A panel of cell biology and biochemistry approaches (reverse transcription quantitative polymerase chain reaction, reporter assays, run-on, polysome fractionation, cross linking immunoprecipitation, filter binding assay, subcellular fractionation, western blotting, immunoprecipitation, stable isotope labeling by amino acids in cell culture) on in vitro-grown primary hepatocytes, human liver cell lines, mouse samples and clinical samples was used. We identify netrin-1 as a hepatic inflammation-inducible factor and decipher its mode of activation through an exhaustive eliminative approach. We show that netrin-1 up-regulation relies on a hitherto unknown mode of induction, namely its exclusive translational activation. This process includes the transfer of NTN1 (netrin-1) mRNA to the endoplasmic reticulum and the direct interaction between the Staufen-1 protein and this transcript as well as netrin-1 mobilization from its cell-bound form. Finally, we explore the impact of a phase 2 clinical trial-tested humanized anti-netrin-1 antibody (NP137) in two distinct, toll-like receptor (TLR) 2/TLR3/TLR6-dependent, hepatic inflammatory mouse settings. We observe a clear anti-inflammatory activity indicating the proinflammatory impact of netrin-1 on several chemokines and Ly6C+ macrophages. CONCLUSIONS: These results identify netrin-1 as an inflammation-inducible factor in the liver through an atypical mechanism as well as its contribution to hepatic inflammation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Vilallongue2022b,

title = {Guidance landscapes unveiled by quantitative proteomics to control reinnervation in adult visual system},

author = {Noemie Vilallongue and Julia Schaeffer and Anne-Marie Hesse and Céline Delpech and Béatrice Blot and Antoine Paccard and Elise Plissonnier and Blandine Excoffier and Yohann Couté and Stephane Belin and Homaira Nawabi},

url = {https://www.nature.com/articles/s41467-022-33799-4},

doi = {10.1038/s41467-022-33799-4},

issn = {2041-1723},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Nature Communications},

volume = {13},

issue = {1},

pages = {6040},

abstract = {Abstract In the injured adult central nervous system (CNS), activation of pro-growth molecular pathways in neurons leads to long-distance regeneration. However, most regenerative fibers display guidance defects, which prevent reinnervation and functional recovery. Therefore, the molecular characterization of the proper target regions of regenerative axons is essential to uncover the modalities of adult reinnervation. In this study, we use mass spectrometry (MS)-based quantitative proteomics to address the proteomes of major nuclei of the adult visual system. These analyses reveal that guidance-associated molecules are expressed in adult visual targets. Moreover, we show that bilateral optic nerve injury modulates the expression of specific proteins. In contrast, the expression of guidance molecules remains steady. Finally, we show that regenerative axons are able to respond to guidance cues ex vivo, suggesting that these molecules possibly interfere with brain target reinnervation in adult. Using a long-distance regeneration model, we further demonstrate that the silencing of specific guidance signaling leads to rerouting of regenerative axons in vivo. Altogether, our results suggest ways to modulate axon guidance of regenerative neurons to achieve circuit repair in adult.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lacroux2022b,

title = {Proteomics unveil a central role for peroxisomes in butyrate assimilation of the heterotrophic Chlorophyte alga Polytomella sp.},

author = {Julien Lacroux and Ariane Atteia and Sabine Brugière and Yohann Couté and Olivier Vallon and Jean-Philippe Steyer and Robert Lis},

url = {https://www.frontiersin.org/articles/10.3389/fmicb.2022.1029828/full},

doi = {10.3389/fmicb.2022.1029828},

issn = {1664-302X},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Frontiers in Microbiology},

volume = {13},

pages = {1029828},

abstract = {Volatile fatty acids found in effluents of the dark fermentation of biowastes can be used for mixotrophic growth of microalgae, improving productivity and reducing the cost of the feedstock. Microalgae can use the acetate in the effluents very well, but butyrate is poorly assimilated and can inhibit growth above 1 gC.L −1 . The non-photosynthetic chlorophyte alga Polytomella sp. SAG 198.80 was found to be able to assimilate butyrate fast. To decipher the metabolic pathways implicated in butyrate assimilation, quantitative proteomics study was developed comparing Polytomella sp. cells grown on acetate and butyrate at 1 gC.L −1 . After statistical analysis, a total of 1772 proteins were retained, of which 119 proteins were found to be overaccumulated on butyrate vs. only 46 on acetate, indicating that butyrate assimilation necessitates additional metabolic steps. The data show that butyrate assimilation occurs in the peroxisome via the β-oxidation pathway to produce acetyl-CoA and further tri/dicarboxylic acids in the glyoxylate cycle. Concomitantly, reactive oxygen species defense enzymes as well as the branched amino acid degradation pathway were strongly induced. Although no clear dedicated butyrate transport mechanism could be inferred, several membrane transporters induced on butyrate are identified as potential condidates. Metabolic responses correspond globally to the increased needs for central cofactors NAD, ATP and CoA, especially in the peroxisome and the cytosol.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Spontaneous Prophage Induction Contributes to the Production of Membrane Vesicles by the Gram-Positive Bacterium Lacticaseibacillus casei BL23},

author = {David Silva Barreira and Pierre Lapaquette and Julia Novion Ducassou and Yohann Couté and Jean Guzzo and Aurélie Rieu},

doi = {10.1128/mbio.02375-22},

issn = {2150-7511},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {mBio},

volume = {13},

issue = {5},

pages = {e0237522},

abstract = {The formation of membrane vesicles (MVs) by Gram-positive bacteria has gained increasing attention over the last decade. Recently, models of vesicle formation have been proposed and involve the digestion of the cell wall by prophage-encoded or stress-induced peptidoglycan (PG) hydrolases and the inhibition of PG synthesis by β-lactam antibiotics. The impact of these mechanisms on vesicle formation is largely dependent on the strain and growth conditions. To date, no information on the production of vesicles by the lactobacilli family has been reported. Here, we aimed to characterize the MVs released by the Gram-positive bacteria Lacticaseibacillus casei BL23 and also investigated the mechanisms involved in vesicle formation. Using electron microscopy, we established that the size of the majority of L. casei BL23 vesicles ranged from 50 to 100 nm. Furthermore, we showed that the vesicles were released consistently throughout the growth of the bacteria in standard culture conditions. The protein composition of the vesicles released in the supernatant was identified and a significant number of prophage proteins was detected. Moreover, using a mutant strain harboring a defective PLE2 prophage, we were able to show that the spontaneous and mitomycin-triggered induction of the prophage PLE2 contribute to the production of MVs by L. casei BL23. Finally, we also demonstrated the influence of prophages on the membrane integrity of bacteria. Overall, our results suggest a key role of the prophage PLE2 in the production of MVs by L. casei BL23 in the absence or presence of genotoxic stress. IMPORTANCE The last few decades have demonstrated that membrane vesicles (MVs) produced by microorganisms can have a wide variety of functions. This diversity places MVs at the crossroads of major research topics in current microbiology such as antibiotic resistance, horizontal gene transfer, cell communication, biofilm development, bacteriophage resistance, and pathogenesis. In particular, vesicles produced by probiotic strains have been shown to play a significant role in their beneficial effects. Thus, the study of vesicle biogenesis is a key element for promoting and improving their release. Overall, our results suggest a key role of spontaneous and mitomycin-triggered prophage induction in MV production by the Gram-positive bacteria Lacticaseibacillus casei BL23. This phenomenon is of great interest as prophage-induced MVs could potentially influence bacterial behavior, stress resistance, and vesicle functions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Fancello2022b,

title = {An analysis of proteogenomics and how and when transcriptome-informed reduction of protein databases can enhance eukaryotic proteomics},

author = {Laura Fancello and Thomas Burger},

doi = {10.1186/s13059-022-02701-2},

issn = {1474-760X},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Genome Biology},

volume = {23},

issue = {1},

pages = {132},

abstract = {BACKGROUND: Proteogenomics aims to identify variant or unknown proteins in bottom-up proteomics, by searching transcriptome- or genome-derived custom protein databases. However, empirical observations reveal that these large proteogenomic databases produce lower-sensitivity peptide identifications. Various strategies have been proposed to avoid this, including the generation of reduced transcriptome-informed protein databases, which only contain proteins whose transcripts are detected in the sample-matched transcriptome. These were found to increase peptide identification sensitivity. Here, we present a detailed evaluation of this approach. RESULTS: We establish that the increased sensitivity in peptide identification is in fact a statistical artifact, directly resulting from the limited capability of target-decoy competition to accurately model incorrect target matches when using excessively small databases. As anti-conservative false discovery rates (FDRs) are likely to hamper the robustness of the resulting biological conclusions, we advocate for alternative FDR control methods that are less sensitive to database size. Nevertheless, reduced transcriptome-informed databases are useful, as they reduce the ambiguity of protein identifications, yielding fewer shared peptides. Furthermore, searching the reference database and subsequently filtering proteins whose transcripts are not expressed reduces protein identification ambiguity to a similar extent, but is more transparent and reproducible. CONCLUSIONS: In summary, using transcriptome information is an interesting strategy that has not been promoted for the right reasons. While the increase in peptide identifications from searching reduced transcriptome-informed databases is an artifact caused by the use of an FDR control method unsuitable to excessively small databases, transcriptome information can reduce the ambiguity of protein identifications.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Abulfaraj2022b,

title = {Analysis of the Arabidopsis coilin mutant reveals a positive role of AtCOILIN in plant immunity},

author = {Aala A Abulfaraj and Hanna M Alhoraibi and Kiruthiga Mariappan and Jean Bigeard and Huoming Zhang and Marilia Almeida-Trapp and Olga Artyukh and Fatimah Abdulhakim and Sabiha Parween and Delphine Pflieger and Ikram Blilou and Heribert Hirt and Naganand Rayapuram},

doi = {10.1093/plphys/kiac280},

issn = {1532-2548},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Plant Physiology},

volume = {190},

issue = {1},

pages = {745-761},

abstract = {Biogenesis of ribonucleoproteins occurs in dynamic subnuclear compartments called Cajal bodies (CBs). COILIN is a critical scaffolding component essential for CB formation, composition, and activity. We recently showed that Arabidopsis (Arabidopsis thaliana) AtCOILIN is phosphorylated in response to bacterial elicitor treatment. Here, we further investigated the role of AtCOILIN in plant innate immunity. Atcoilin mutants are compromised in defense responses to bacterial pathogens. Besides confirming a role of AtCOILIN in alternative splicing (AS), Atcoilin showed differential expression of genes that are distinct from those of AS, including factors involved in RNA biogenesis, metabolism, plant immunity, and phytohormones. Atcoilin mutant plants have reduced levels of defense phytohormones. As expected, the mutant plants were more sensitive to the necrotrophic fungal pathogen Botrytis cinerea. Our findings reveal an important role for AtCOILIN in innate plant immunity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {The Toxoplasma effector GRA28 promotes parasite dissemination by inducing dendritic cell-like migratory properties in infected macrophages},

author = {Arne L Ten Hoeve and Laurence Braun and Matias E Rodriguez and Gabriela C Olivera and Alexandre Bougdour and Lucid Belmudes and Yohann Couté and Jeroen P J Saeij and Mohamed-Ali Hakimi and Antonio Barragan},

doi = {10.1016/j.chom.2022.10.001},

issn = {1934-6069},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Cell Host & Microbe},

volume = {30},

issue = {11},

pages = {1570–1588.e7},

abstract = {Upon pathogen detection, macrophages normally stay sessile in tissues while dendritic cells (DCs) migrate to secondary lymphoid tissues. The obligate intracellular protozoan Toxoplasma gondii exploits the trafficking of mononuclear phagocytes for dissemination via unclear mechanisms. We report that, upon T. gondii infection, macrophages initiate the expression of transcription factors normally attributed to DCs, upregulate CCR7 expression with a chemotactic response, and perform systemic migration when adoptively transferred into mice. We show that parasite effector GRA28, released by the MYR1 secretory pathway, cooperates with host chromatin remodelers in the host cell nucleus to drive the chemotactic migration of parasitized macrophages. During in vivo challenge studies, bone marrow-derived macrophages infected with wild-type T. gondii outcompeted those challenged with MYR1- or GRA28-deficient strains in migrating and reaching secondary organs. This work reveals how an intracellular parasite hijacks chemotaxis in phagocytes and highlights a remarkable migratory plasticity in differentiated cells of the mononuclear phagocyte system.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Leisico2022b,

title = {Structure of the human heparan sulfate polymerase complex EXT1-EXT2},

author = {Francisco Leisico and Juneina Omeiri and Christine Le Narvor and Joël Beaudouin and Michael Hons and Daphna Fenel and Guy Schoehn and Yohann Couté and David Bonnaffé and Rabia Sadir and Hugues Lortat-Jacob and Rebekka Wild},

doi = {10.1038/s41467-022-34882-6},

issn = {2041-1723},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Nature Communications},

volume = {13},

issue = {1},

pages = {7110},

abstract = {Heparan sulfates are complex polysaccharides that mediate the interaction with a broad range of protein ligands at the cell surface. A key step in heparan sulfate biosynthesis is catalyzed by the bi-functional glycosyltransferases EXT1 and EXT2, which generate the glycan backbone consisting of repeating N-acetylglucosamine and glucuronic acid units. The molecular mechanism of heparan sulfate chain polymerization remains, however, unknown. Here, we present the cryo-electron microscopy structure of human EXT1-EXT2, which reveals the formation of a tightly packed hetero-dimeric complex harboring four glycosyltransferase domains. A combination of in vitro and in cellulo mutational studies is used to dissect the functional role of the four catalytic sites. While EXT1 can catalyze both glycosyltransferase reactions, our results indicate that EXT2 might only have N-acetylglucosamine transferase activity. Our findings provide mechanistic insight into heparan sulfate chain elongation as a nonprocessive process and lay the foundation for future studies on EXT1-EXT2 function in health and disease.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lupette2022b,

title = {Quantitative proteomic analyses reveal the impact of nitrogen starvation on the proteome of the model diatom Phaeodactylum tricornutum},

author = {Josselin Lupette and Marianne Tardif and Sabine Brugière and Yohann Couté and Juliette Salvaing and Eric Maréchal},

doi = {10.1002/pmic.202200155},

issn = {1615-9861},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Proteomics},

volume = {22},

issue = {22},

pages = {e2200155},

abstract = {Diatoms are one of the largest groups in phytoplankton biodiversity. Understanding their response to nitrogen variations, present from micromolar to near-zero levels in oceans and fresh waters, is essential to comprehend their ecological success. Nitrogen starvation is used in biotechnological processes, to trigger the remodeling of carbon metabolism in the direction of fatty acids and triacylglycerol synthesis. We evaluated whole proteome changes in Phaeodactylum tricornutum after 7 days of cultivation with 5.5-mM nitrate (+N) or without any nitrogen source (-N). On a total of 3768 proteins detected in biological replicates, our analysis pointed to 384 differentially abundant proteins (DAP). Analysis of proteins of lower abundance in -N revealed an arrest of amino acid and protein syntheses, a remodeling of nitrogen metabolism, and a decrease of the proteasome abundance suggesting a decline in unselective whole-proteome decay. Analysis of proteins of higher abundance revealed the setting up of a general nitrogen scavenging system dependent on deaminases. The increase of a plastid palmitoyl-ACP desaturase appeared as a hallmark of carbon metabolism rewiring in the direction of fatty acid and triacylglycerol synthesis. This dataset is also valuable to select gene candidates for improved biotechnological properties.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Timcheva2022b,

title = {Chromatin-associated YTHDC1 coordinates heat-induced reprogramming of gene expression},

author = {Kalina Timcheva and Solenne Dufour and Leila Touat-Todeschini and Callum Burnard and Marie-Christine Carpentier and Florent Chuffart and Rémy Merret and Marion Helsmoortel and Sabrina Ferré and Aude Grézy and Yohann Couté and Sophie Rousseaux and Saadi Khochbin and Claire Vourc’h and Cécile Bousquet-Antonelli and Rosemary Kiernan and Daphné Seigneurin-Berny and André Verdel},

url = {https://linkinghub.elsevier.com/retrieve/pii/S2211124722016722},

doi = {10.1016/j.celrep.2022.111784},

issn = {22111247},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Cell Reports},

volume = {41},

issue = {11},

pages = {111784},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Etourneau2022b,

title = {Challenging Targets or Describing Mismatches? A Comment on Common Decoy Distribution by Madej et al},

author = {Lucas Etourneau and Thomas Burger},

doi = {10.1021/acs.jproteome.2c00279},

issn = {1535-3907},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Journal of Proteome Research},

volume = {21},

issue = {12},

pages = {2840-2845},

abstract = {In their recent article, Madej et al. (Madej, D.; Wu, L.; Lam, H.Common Decoy Distributions Simplify False Discovery Rate Estimation in Shotgun Proteomics. J. Proteome Res.2022, 21 (2), 339-348) proposed an original way to solve the recurrent issue of controlling for the false discovery rate (FDR) in peptide-spectrum-match (PSM) validation. Briefly, they proposed to derive a single precise distribution of decoy matches termed the Common Decoy Distribution (CDD) and to use it to control for FDR during a target-only search. Conceptually, this approach is appealing as it takes the best of two worlds, i.e., decoy-based approaches (which leverage a large-scale collection of empirical mismatches) and decoy-free approaches (which are not subject to the randomness of decoy generation while sparing an additional database search). Interestingly, CDD also corresponds to a middle-of-the-road approach in statistics with respect to the two main families of FDR control procedures: Although historically based on estimating the false-positive distribution, FDR control has recently been demonstrated to be possible thanks to competition between the original variables (in proteomics, target sequences) and their fictional counterparts (in proteomics, decoys). Discriminating between these two theoretical trends is of prime importance for computational proteomics. In addition to highlighting why proteomics was a source of inspiration for theoretical biostatistics, it provides practical insights into the improvements that can be made to FDR control methods used in proteomics, including CDD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lai2022b,

title = {Characterizing Nanoparticle Mass Distributions Using Charge-Independent Nanoresonator Mass Spectrometry},

author = {Szu-Hsueh Lai and Adrien Reynaud and Ning-Ning Zhang and Minjeong Kwak and Bogdan Vysotskyi and Sergio Dominguez-Medina and Thomas Fortin and Kavya Clement and Martial Defoort and Tae Geol Lee and Kun Liu and Sébastien Hentz and Christophe D Masselon},

url = {https://pubs.acs.org/doi/10.1021/acs.jpcc.2c06675},

doi = {10.1021/acs.jpcc.2c06675},

issn = {1932-7447, 1932-7455},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {The Journal of Physical Chemistry C},

volume = {126},

issue = {49},

pages = {20946-20953},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Targeted Proteomics Analysis of Staphylococcal Superantigenic Toxins in Menstrual Fluid from Women with Menstrual Toxic Shock Syndrome (mTSS)},

author = {Marie Courçon and Cédric Badiou and Mathilde Louwagie and Sibyle Etievant and Michel Jaquinod and Gérard Lina and Virginie Brun},

url = {https://www.mdpi.com/2072-6651/14/12/886},

doi = {10.3390/toxins14120886},

issn = {2072-6651},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Toxins},

volume = {14},

issue = {12},

pages = {886},

abstract = {Menstrual toxic shock syndrome (mTSS) is a rare life-threatening febrile illness that occurs in women using intravaginal menstrual protection. It is caused by toxic shock syndrome toxin 1 (TSST-1) produced by Staphylococcus aureus, triggering a sudden onset of rash and hypotension, subsequently leading to multiple organ failure. Detecting TSST-1 and S. aureus virulence factors in menstrual fluid could accelerate the diagnosis and improve therapeutic management of mTSS. However, menstrual fluid is a highly complex matrix, making detection of bacterial toxins challenging. Here, we present a mass-spectrometry-based proteomics workflow for the targeted, quantitative analysis of four S. aureus superantigenic toxins in menstrual fluids (TSST-1, SEA, SEC, and SED). This method was applied to characterize toxin levels in menstrual fluids collected from patients with mTSS and healthy women. Toxins were detectable in samples from patients with mTSS and one healthy donor at concentrations ranging from 0 to 0.46 µg/mL for TSST-1, and 0 to 1.07 µg/mL for SEC. SEA and SED were never detected in clinical specimens, even though many S. aureus strains were positive for the corresponding genes. The method presented here could be used to explore toxin production in vivo in users of intravaginal devices to improve the diagnosis, understanding, and prevention of mTSS.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Caron2022b,

title = {Loss of SET1/COMPASS methyltransferase activity reduces lifespan and fertility in Caenorhabditis elegans},

author = {Matthieu Caron and Loïc Gely and Steven Garvis and Annie Adrait and Yohann Couté and Francesca Palladino and Paola Fabrizio},

doi = {10.26508/lsa.202101140},

issn = {2575-1077},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Life Science Alliance},

volume = {5},

issue = {3},

pages = {e202101140},

abstract = {Changes in histone post-translational modifications are associated with aging through poorly defined mechanisms. Histone 3 lysine 4 (H3K4) methylation at promoters is deposited by SET1 family methyltransferases acting within conserved multiprotein complexes known as COMPASS. Previous work yielded conflicting results about the requirement for H3K4 methylation during aging. Here, we reassessed the role of SET1/COMPASS-dependent H3K4 methylation in Caenorhabditis elegans lifespan and fertility by generating set-2(syb2085) mutant animals that express a catalytically inactive form of SET-2, the C. elegans SET1 homolog. We show that set-2(syb2085) animals retain the ability to form COMPASS, but have a marked global loss of H3K4 di- and trimethylation (H3K4me2/3). Reduced H3K4 methylation was accompanied by loss of fertility, as expected; however, in contrast to earlier studies, set-2(syb2085) mutants displayed a significantly shortened, not extended, lifespan and had normal intestinal fat stores. Other commonly used set-2 mutants were also short-lived, as was a cfp-1 mutant that lacks the SET1/COMPASS chromatin-targeting component. These results challenge previously held views and establish that WT H3K4me2/3 levels are essential for normal lifespan in C. elegans.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Ielasi2022b,

title = {Human histone pre-mRNA assembles histone or canonical mRNA-processing complexes by overlapping 3'-end sequence elements},

author = {Francesco S Ielasi and Sara Ternifi and Emeline Fontaine and Domenico Iuso and Yohann Couté and Andrés Palencia},

doi = {10.1093/nar/gkac878},

issn = {1362-4962},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Nucleic Acids Research},

volume = {50},

issue = {21},

pages = {12425-12443},

abstract = {Human pre-mRNA processing relies on multi-subunit macromolecular complexes, which recognize specific RNA sequence elements essential for assembly and activity. Canonical pre-mRNA processing proceeds via the recognition of a polyadenylation signal (PAS) and a downstream sequence element (DSE), and produces polyadenylated mature mRNAs, while replication-dependent (RD) histone pre-mRNA processing requires association with a stem-loop (SL) motif and a histone downstream element (HDE), and produces cleaved but non-polyadenylated mature mRNAs. H2AC18 mRNA, a specific H2A RD histone pre-mRNA, can be processed to give either a non-polyadenylated mRNA, ending at the histone SL, or a polyadenylated mRNA. Here, we reveal how H2AC18 captures the two human pre-mRNA processing complexes in a mutually exclusive mode by overlapping a canonical PAS (AAUAAA) sequence element with a HDE. Disruption of the PAS sequence on H2AC18 pre-mRNA prevents recruitment of the canonical complex in vitro, without affecting the histone machinery. This shows how the relative position of cis-acting elements in histone pre-mRNAs allows the selective recruitment of distinct human pre-mRNA complexes, thereby expanding the capability to regulate 3' processing and polyadenylation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Binda2022b,

title = {SMA-linked SMN mutants prevent phase separation properties and SMN interactions with FMRP family members},

author = {Olivier Binda and Franceline Juillard and Julia Novion Ducassou and Constance Kleijwegt and Geneviève Paris and Andréanne Didillon and Faouzi Baklouti and Armelle Corpet and Yohann Couté and Jocelyn Côté and Patrick Lomonte},

doi = {10.26508/lsa.202201429},

issn = {2575-1077},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Life Science Alliance},

volume = {6},

issue = {1},

pages = {e202201429},

abstract = {Although recent advances in gene therapy provide hope for spinal muscular atrophy (SMA) patients, the pathology remains the leading genetic cause of infant mortality. SMA is a monogenic pathology that originates from the loss of the SMN1 gene in most cases or mutations in rare cases. Interestingly, several SMN1 mutations occur within the TUDOR methylarginine reader domain of SMN. We hypothesized that in SMN1 mutant cases, SMA may emerge from aberrant protein-protein interactions between SMN and key neuronal factors. Using a BioID proteomic approach, we have identified and validated a number of SMN-interacting proteins, including fragile X mental retardation protein (FMRP) family members (FMRFM). Importantly, SMA-linked SMNTUDOR mutant forms (SMNST) failed to interact with FMRFM In agreement with the recent work, we define biochemically that SMN forms droplets in vitro and these droplets are stabilized by RNA, suggesting that SMN could be involved in the formation of membraneless organelles, such as Cajal nuclear bodies. Finally, we found that SMN and FMRP co-fractionate with polysomes, in an RNA-dependent manner, suggesting a potential role in localized translation in motor neurons.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{boulan_crmp4-mediated_2021,

title = {CRMP4-mediated fornix development involves semaphorin-3E signaling pathway},

author = {Benoît Boulan and Charlotte Ravanello and Amandine Peyrel and Christophe Bosc and Christian Delphin and Florence Appaix and Eric Denarier and Alexandra Kraut and Muriel Jaquier-Sarlin and Alyson Fournier and Annie Andrieux and Sylvie Gory-Fauré and Jean-Christophe Deloulme},

url = {https://elifesciences.org/articles/70361},

doi = {10.7554/eLife.70361},

issn = {2050-084X},

year  = {2021},

date = {2021-12-01},

urldate = {2021-12-01},

journal = {eLife},

volume = {10},

pages = {e70361},

abstract = {Neurodevelopmental axonal pathfinding plays a central role in correct brain wiring and subsequent cognitive abilities. Within the growth cone, various intracellular effectors transduce axonal guidance signals by remodeling the cytoskeleton. Semaphorin-3E (Sema3E) is a guidance cue implicated in development of the fornix, a neuronal tract connecting the hippocampus to the hypothalamus. Microtubule-Associated Protein 6 (MAP6) has been shown to be involved in the Sema3E growth-promoting signaling pathway. In this study, we identified the Collapsin Response Mediator Protein 4 (CRMP4) as a MAP6 partner and a crucial effector in Sema3E growth-promoting activity. CRMP4-KO mice displayed abnormal fornix development reminiscent of that observed in Sema3E-KO mice. CRMP4 was shown to interact with the Sema3E tripartite receptor complex within Detergent- 

 Resistant 

 Membrane (DRM) domains, and DRM domain integrity was required to transduce Sema3E signaling through the Akt/GSK3 pathway. Finally, we showed that the cytoskeleton-binding domain of CRMP4 is required for Sema3E's growth-promoting activity, suggesting that CRMP4 plays a role at the interface between Sema3E receptors, located in DRM domains, and the cytoskeleton network. As the fornix is affected in many psychiatric diseases, such as schizophrenia, our results provide new insights to better understand the neurodevelopmental components of these diseases.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ropers_multiomics_2021,

title = {Multiomics Study of Bacterial Growth Arrest in a Synthetic Biology Application},

author = {Delphine Ropers and Yohann Couté and Laëtitia Faure and Sabrina Ferré and Delphine Labourdette and Arieta Shabani and Lidwine Trouilh and Perrine Vasseur and Gwénaëlle Corre and Myriam Ferro and Marie-Ange Teste and Johannes Geiselmann and Hidde Jong},

doi = {10.1021/acssynbio.1c00115},

issn = {2161-5063},

year  = {2021},

date = {2021-11-01},

urldate = {2021-11-01},

journal = {ACS synthetic biology},

abstract = {We investigated the scalability of a previously developed growth switch based on external control of RNA polymerase expression. Our results indicate that, in liter-scale bioreactors operating in fed-batch mode, growth-arrested Escherichia coli cells are able to convert glucose to glycerol at an increased yield. A multiomics quantification of the physiology of the cells shows that, apart from acetate production, few metabolic side effects occur. However, a number of specific responses to growth slow-down and growth arrest are launched at the transcriptional level. These notably include the downregulation of genes involved in growth-associated processes, such as amino acid and nucleotide metabolism and translation. Interestingly, the transcriptional responses are buffered at the proteome level, probably due to the strong decrease of the total mRNA concentration after the diminution of transcriptional activity and the absence of growth dilution of proteins. Growth arrest thus reduces the opportunities for dynamically adjusting the proteome composition, which poses constraints on the design of biotechnological production processes but may also avoid the initiation of deleterious stress responses.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{jalabert_profiling_2021,

title = {Profiling of ob/ob mice skeletal muscle exosome-like vesicles demonstrates combined action of miRNAs, proteins and lipids to modulate lipid homeostasis in recipient cells},

author = {Audrey Jalabert and Laura Reininger and Emmanuelle Berger and Yohann Coute and Emmanuelle Meugnier and Alexis Forterre and Elizabeth Errazuriz-Cerda and Alain Geloen and Myriam Aouadi and Karim Bouzakri and Jennifer Rieusset and Sophie Rome},

doi = {10.1038/s41598-021-00983-3},

issn = {2045-2322},

year  = {2021},

date = {2021-11-01},

urldate = {2021-11-01},

journal = {Scientific Reports},

volume = {11},

number = {1},

pages = {21626},

abstract = {We have determined the lipid, protein and miRNA composition of skeletal muscle (SkM)-released extracellular vesicles (ELVs) from Ob/ob (OB) vs wild-type (WT) mice. The results showed that atrophic insulin-resistant OB-SkM released less ELVs than WT-SkM, highlighted by a RAB35 decrease and an increase in intramuscular cholesterol content. Proteomic analyses of OB-ELVs revealed a group of 37 proteins functionally connected, involved in lipid oxidation and with catalytic activities. OB-ELVs had modified contents for phosphatidylcholine (PC 34-4, PC 40-3 and PC 34-0), sphingomyelin (Sm d18:1/18:1) and ceramides (Cer d18:1/18:0) and were enriched in cholesterol, likely to alleviated intracellular accumulation. Surprisingly many ELV miRNAs had a nuclear addressing sequence, and targeted genes encoding proteins with nuclear activities. Interestingly, SkM-ELV miRNA did not target mitochondria. The most significant function targeted by the 7 miRNAs altered in OB-ELVs was lipid metabolism. In agreement, OB-ELVs induced lipid storage in recipient adipocytes and increased lipid up-take and fatty acid oxidation in recipient muscle cells. In addition, OB-ELVs altered insulin-sensitivity and induced atrophy in muscle cells, reproducing the phenotype of the releasing OB muscles. These data suggest for the first time, a cross-talk between muscle cells and adipocytes, through the SkM-ELV route, in favor of adipose tissue expansion.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{hage_complex_2021,

title = {The Complex Regulatory Role of Cytomegalovirus Nuclear Egress Protein pUL50 in the Production of Infectious Virus},

author = {Sigrun Häge and Nicole Büscher and Victoria Pakulska and Friedrich Hahn and Annie Adrait and Steffi Krauter and Eva Maria Borst and Ursula Schlötzer-Schrehardt and Yohann Couté and Bodo Plachter and Manfred Marschall},

url = {https://www.mdpi.com/2073-4409/10/11/3119},

doi = {10.3390/cells10113119},

issn = {2073-4409},

year  = {2021},

date = {2021-11-01},

urldate = {2021-11-01},

journal = {Cells},

volume = {10},

number = {11},

pages = {3119},

abstract = {The regulation of the nucleocytoplasmic release of herpesviral capsids is defined by the process of nuclear egress. Due to their large size, nuclear capsids are unable to traverse via nuclear pores, so that herpesviruses evolved to develop a vesicular transport pathway mediating their transition through both leaflets of the nuclear membrane. This process involves regulatory proteins, which support the local distortion of the nuclear envelope. For human cytomegalovirus (HCMV), the nuclear egress complex (NEC) is determined by the pUL50-pUL53 core that initiates multicomponent assembly with NEC-associated proteins and capsids. Hereby, pUL50 serves as a multi-interacting determinant that recruits several viral and cellular factors by direct and indirect contacts. Recently, we generated an ORF-UL50-deleted recombinant HCMV in pUL50-complementing cells and obtained first indications of putative additional functions of pUL50. In this study, we produced purified ΔUL50 particles under both complementing (ΔUL50C) and non-complementing (ΔUL50N) conditions and performed a phenotypical characterization. Findings were as follows: (i) ΔUL50N particle preparations exhibited a clear replicative defect in qPCR-based infection kinetics compared to ΔUL50C particles; (ii) immuno-EM analysis of ΔUL50C did not reveal major changes in nuclear distribution of pUL53 and lamin A/C; (iii) mass spectrometry-based quantitative proteomics showed a large concordance of protein contents in the NIEP fractions of ΔUL50C and ΔUL50N particles, but virion fraction was close to the detection limit for ΔUL50N; (iv) confocal imaging of viral marker proteins of immediate early (IE) and later phases of ΔUL50N infection indicated a very low number of cells showing an onset of viral lytic protein expression; and, finally (v) quantitative measurements of encapsidated genomes provided evidence for a substantial reduction in the DNA contents in ΔUL50N compared to ΔUL50C particles. In summary, the results point to a complex and important regulatory role of the HCMV nuclear egress protein pUL50 in the maturation of infectious virus.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{capizzi_developmental_2021,

title = {Developmental defects in Huntington’s disease show that axonal growth and microtubule reorganization require NUMA1},

author = {Mariacristina Capizzi and Rémi Carpentier and Eric Denarier and Annie Adrait and Rayane Kassem and Marina Mapelli and Yohann Couté and Sandrine Humbert},

url = {https://linkinghub.elsevier.com/retrieve/pii/S0896627321008631},

doi = {10.1016/j.neuron.2021.10.033},

issn = {08966273},

year  = {2021},

date = {2021-11-01},

urldate = {2021-11-01},

journal = {Neuron},

pages = {S0896627321008631},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{bouroumeau_cyclon_2021,

title = {CYCLON and NPM1 Cooperate within an Oncogenic Network Predictive of R-CHOP Response in DLBCL},

author = {Antonin Bouroumeau and Lucile Bussot and Sieme Hamaidia and Andrea Garcìa-Sandoval and Anna Bergan-Dahl and Patricia Betton-Fraisse and Samuel Duley and Cyril Fournier and Romain Aucagne and Annie Adrait and Yohann Couté and Anne McLeer and Edwige Col and Laurence David-Boudet and Tatiana Raskovalova and Marie-Christine Jacob and Claire Vettier and Simon Chevalier and Sylvain Carras and Christine Lefebvre and Caroline Algrin and Rémy Gressin and Mary B. Callanan and Hervé Sartelet and Thierry Bonnefoix and Anouk Emadali},

url = {https://www.mdpi.com/2072-6694/13/23/5900},

doi = {10.3390/cancers13235900},

issn = {2072-6694},

year  = {2021},

date = {2021-11-01},

urldate = {2021-11-01},

journal = {Cancers},

volume = {13},

number = {23},

pages = {5900},

abstract = {R-CHOP immuno-chemotherapy significantly improved clinical management of diffuse large B-cell lymphoma (DLBCL). However, 30–40% of DLBCL patients still present a refractory disease or relapse. Most of the prognostic markers identified to date fail to accurately stratify high-risk DLBCL patients. We have previously shown that the nuclear protein CYCLON is associated with DLBCL disease progression and resistance to anti-CD20 immunotherapy in preclinical models. We also recently reported that it also represents a potent predictor of refractory disease and relapse in a retrospective DLBCL cohort. However, only sparse data are available to predict the potential biological role of CYCLON and how it might exert its adverse effects on lymphoma cells. Here, we characterized the protein interaction network of CYCLON, connecting this protein to the nucleolus, RNA processing, MYC signaling and cell cycle progression. Among this network, NPM1, a nucleolar multi-functional protein frequently deregulated in cancer, emerged as another potential target related to treatment resistance in DLBCL. Immunohistochemistry evaluation of CYCLON and NPM1 revealed that their co-expression is strongly related to inferior prognosis in DLBCL. More specifically, alternative sub-cellular localizations of the proteins (extra-nucleolar CYCLON and pan-cellular NPM1) represent independent predictive factors specifically associated to R-CHOP refractory DLBCL patients, which could allow them to be orientated towards risk-adapted or novel targeted therapies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pailleux_mass_2021,

title = {Mass Spectrometry-Based Proteomics Reveal Alcohol Dehydrogenase 1B as a Blood Biomarker Candidate to Monitor Acetaminophen-Induced Liver Injury},

author = {Floriane Pailleux and Pauline Maes and Michel Jaquinod and Justine Barthelon and Marion Darnaud and Claire Lacoste and Yves Vandenbrouck and Benoît Gilquin and Mathilde Louwagie and Anne-Marie Hesse and Alexandra Kraut and Jérôme Garin and Vincent Leroy and Jean-Pierre Zarski and Christophe Bruley and Yohann Couté and Didier Samuel and Philippe Ichai and Jamila Faivre and Virginie Brun},

url = {https://www.mdpi.com/1422-0067/22/20/11071},

doi = {10.3390/ijms222011071},

issn = {1422-0067},

year  = {2021},

date = {2021-10-01},

urldate = {2021-10-01},

journal = {International Journal of Molecular Sciences},

volume = {22},

number = {20},

pages = {11071},

abstract = {Acute liver injury (ALI) is a severe disorder resulting from excessive hepatocyte cell death, and frequently caused by acetaminophen intoxication. Clinical management of ALI progression is hampered by the dearth of blood biomarkers available. In this study, a bioinformatics workflow was developed to screen omics databases and identify potential biomarkers for hepatocyte cell death. Then, discovery proteomics was harnessed to select from among these candidates those that were specifically detected in the blood of acetaminophen-induced ALI patients. Among these candidates, the isoenzyme alcohol dehydrogenase 1B (ADH1B) was massively leaked into the blood. To evaluate ADH1B, we developed a targeted proteomics assay and quantified ADH1B in serum samples collected at different times from 17 patients admitted for acetaminophen-induced ALI. Serum ADH1B concentrations increased markedly during the acute phase of the disease, and dropped to undetectable levels during recovery. In contrast to alanine aminotransferase activity, the rapid drop in circulating ADH1B concentrations was followed by an improvement in the international normalized ratio (INR) within 10–48 h, and was associated with favorable outcomes. In conclusion, the combination of omics data exploration and proteomics revealed ADH1B as a new blood biomarker candidate that could be useful for the monitoring of acetaminophen-induced ALI.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{deutsch_advances_2021,

title = {Advances and Utility of the Human Plasma Proteome},

author = {Eric W. Deutsch and Gilbert S. Omenn and Zhi Sun and Michal Maes and Maria Pernemalm and Krishnan K. Palaniappan and Natasha Letunica and Yves Vandenbrouck and Virginie Brun and Sheng-ce Tao and Xiaobo Yu and Philipp E. Geyer and Vera Ignjatovic and Robert L. Moritz and Jochen M. Schwenk},

url = {https://doi.org/10.1021/acs.jproteome.1c00657},

doi = {10.1021/acs.jproteome.1c00657},

issn = {1535-3893},

year  = {2021},

date = {2021-10-01},

urldate = {2021-10-01},

journal = {Journal of Proteome Research},

abstract = {The study of proteins circulating in blood offers tremendous opportunities to diagnose, stratify, or possibly prevent diseases. With recent technological advances and the urgent need to understand the effects of COVID-19, the proteomic analysis of blood-derived serum and plasma has become even more important for studying human biology and pathophysiology. Here we provide views and perspectives about technological developments and possible clinical applications that use mass-spectrometry(MS)- or affinity-based methods. We discuss examples where plasma proteomics contributed valuable insights into SARS-CoV-2 infections, aging, and hemostasis and the opportunities offered by combining proteomics with genetic data. As a contribution to the Human Proteome Organization (HUPO) Human Plasma Proteome Project (HPPP), we present the Human Plasma PeptideAtlas build 2021-07 that comprises 4395 canonical and 1482 additional nonredundant human proteins detected in 240 MS-based experiments. In addition, we report the new Human Extracellular Vesicle PeptideAtlas 2021-06, which comprises five studies and 2757 canonical proteins detected in extracellular vesicles circulating in blood, of which 74% (2047) are in common with the plasma PeptideAtlas. Our overview summarizes the recent advances, impactful applications, and ongoing challenges for translating plasma proteomics into utility for precision medicine.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{fortin_nonlinear_2021,

title = {A nonlinear model for nano-electro mechanical mass sensing signals processing},

author = {T. Fortin and B. Vysotskyi and M. Defoort and A. Reynaud and S. -H. Lai and S. Dominguez-Medina and K. Clement and V. Cumaku and S. Hentz and C. Masselon},

url = {https://ieeexplore.ieee.org/document/9509545/},

doi = {10.1109/JSEN.2021.3103713},

issn = {1530-437X, 1558-1748, 2379-9153},

year  = {2021},

date = {2021-08-01},

urldate = {2021-08-01},

journal = {IEEE Sensors Journal},

pages = {1--1},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{permiakova_sketched_2021,

title = {Sketched Stochastic Dictionary Learning for large‐scale data and application to high‐throughput mass spectrometry},

author = {Olga Permiakova and Thomas Burger},

url = {https://onlinelibrary.wiley.com/doi/10.1002/sam.11542},

doi = {10.1002/sam.11542},

issn = {1932-1864, 1932-1872},

year  = {2021},

date = {2021-08-01},

urldate = {2021-08-01},

journal = {Statistical Analysis and Data Mining: The ASA Data Science Journal},

pages = {sam.11542},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{gloaguen_chlorokb_2021,

title = {ChloroKB, a cell metabolism reconstruction of the model plant Arabidopsis thaliana},

author = {Pauline Gloaguen and Yves Vandenbrouck and Jacques Joyard and Gilles Curien},

url = {https://comptes-rendus.academie-sciences.fr/biologies/articles/10.5802/crbiol.49/},

doi = {10.5802/crbiol.49},

issn = {1768-3238},

year  = {2021},

date = {2021-07-01},

urldate = {2021-07-01},

journal = {Comptes Rendus. Biologies},

volume = {344},

number = {2},

pages = {157--163},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{clement_requirements_2021,

title = {Requirements and attributes of nano-resonator mass spectrometry for the analysis of intact viral particles},

author = {Kavya Clement and Adrien Reynaud and Martial Defoort and Bogdan Vysotskyi and Thomas Fortin and Szu-Hsueh Lai and Vaitson Çumaku and Sergio Dominguez-Medina and Sébastien Hentz and Christophe Masselon},

url = {https://link.springer.com/10.1007/s00216-021-03511-4},

doi = {10.1007/s00216-021-03511-4},

issn = {1618-2642, 1618-2650},

year  = {2021},

date = {2021-07-01},

urldate = {2021-07-01},

journal = {Analytical and Bioanalytical Chemistry},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{farhat_plant-like_2021,

title = {A plant-like mechanism coupling m6A reading to polyadenylation safeguards transcriptome integrity and developmental gene partitioning in Toxoplasma},

author = {Dayana C Farhat and Matthew W Bowler and Guillaume Communie and Dominique Pontier and Lucid Belmudes and Caroline Mas and Charlotte Corrao and Yohann Couté and Alexandre Bougdour and Thierry Lagrange and Mohamed-ali Hakimi and Christopher Swale},

url = {https://elifesciences.org/articles/68312},

doi = {10.7554/eLife.68312},

issn = {2050-084X},

year  = {2021},

date = {2021-07-01},

urldate = {2021-07-01},

journal = {eLife},

volume = {10},

pages = {e68312},

abstract = {Correct 3'end processing of mRNAs is one of the regulatory cornerstones of gene expression. In a parasite that must adapt to the regulatory requirements of its multi-host life style, there is a need to adopt additional means to partition the distinct transcriptional signatures of the closely and tandemly-arranged stage specific genes. In this study, we report our findings in 

 T. gondii 

 of an m6A-dependent 3'end polyadenylation serving as a transcriptional barrier at these 

 loci 

 . We identify the core polyadenylation complex within 

 T. gondii 

 and establish CPSF4 as a reader for m6A-modified mRNAs, via a YTH domain within its C-terminus, a feature which is shared with plants. We bring evidence of the specificity of this interaction both biochemically, and by determining the crystal structure at high resolution of the 

 T. gondii 

 CPSF4-YTH in complex with an m6A modified RNA. We show that the loss of m6A, both at the level of its deposition or its recognition was associated with an increase in aberrantly elongated chimeric mRNAs emanating from impaired transcriptional termination, a phenotype previously noticed in the plant model 

 Arabidopsis thaliana 

 . Nanopore direct RNA sequencing shows the occurrence of transcriptional read-through breaching into downstream repressed stage-specific genes, in the absence of either CPSF4 or the m6A RNA methylase components in both 

 T. gondii 

 and 

 A. thaliana 

 . Taken together, our results shed light on an essential regulatory mechanism coupling the pathways of m6A metabolism directly to the cleavage and polyadenylation processes, one that interestingly seem to serve, in both 

 T. gondii 

 and 

 A. thaliana 

 , as a guardian against aberrant transcriptional read-throughs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{notaro_expanding_2021,

title = {Expanding the occurrence of polysaccharides to the viral world: the case of Mimivirus},

author = {Anna Notaro and Yohann Couté and Lucid Belmudes and Maria Elena Laugieri and Annalisa Salis and Gianluca Damonte and Antonio Molinaro and Michela Tonetti and Chantal Abergel and Cristina De Castro},

url = {https://onlinelibrary.wiley.com/doi/10.1002/anie.202106671},

doi = {10.1002/anie.202106671},

issn = {1433-7851, 1521-3773},

year  = {2021},

date = {2021-07-01},

urldate = {2021-07-01},

journal = {Angewandte Chemie International Edition},

pages = {anie.202106671},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{do_argonaute_2021,

title = {Argonaute Autoantibodies as Biomarkers in Autoimmune Neurologic Diseases},

author = {Le-Duy Do and Christian P. Moritz and Sergio Muñiz-Castrillo and Anne-Laurie Pinto and Yannick Tholance and Sabine Brugiere and Yohann Couté and Oda Stoevesandt and Michael J. Taussig and Véronique Rogemond and Alberto Vogrig and Bastien Joubert and Karine Ferraud and Jean-Philippe Camdessanché and Jean-Christophe Antoine and Jérôme Honnorat},

url = {http://nn.neurology.org/lookup/doi/10.1212/NXI.0000000000001032},

doi = {10.1212/NXI.0000000000001032},

issn = {2332-7812},

year  = {2021},

date = {2021-07-01},

urldate = {2021-07-01},

journal = {Neurology - Neuroimmunology Neuroinflammation},

volume = {8},

number = {5},

pages = {e1032},

abstract = {Objective 

 To identify and characterize autoantibodies (Abs) as novel biomarkers for an autoimmune context in patients with central and peripheral neurologic diseases. 

 

 

 Methods 

 Two distinct approaches (immunoprecipitation/mass spectrometry–based proteomics and protein microarrays) and patients' sera and CSF were used. The specificity of the identified target was confirmed by cell-based assay (CBA) in 856 control samples. 

 

 

 Results 

 Using the 2 methods as well as sera and CSF of patients with central and peripheral neurologic involvement, we identified Abs against the family of Argonaute proteins (mainly AGO1 and AGO2), which were already reported in systemic autoimmunity. AGO-Abs were mostly of immunoglobulin G 1 subclass and conformation dependent. Using CBA, AGO-Abs were detected in 21 patients with a high suspicion of autoimmune neurologic diseases (71.4% were women; median age 57 years) and only in 4/856 (0.5%) controls analyzed by CBA (1 diagnosed with small-cell lung cancer and the other 3 with Sjögren syndrome). Among the 21 neurologic patients identified, the main clinical presentations were sensory neuronopathy (8/21, 38.1%) and limbic encephalitis (6/21, 28.6%). Fourteen patients (66.7%) had autoimmune comorbidities and/or co-occurring Abs, whereas AGO-Abs were the only autoimmune biomarker for the remaining 7/21 (33.3%). Thirteen (61.9%) patients were treated with immunotherapy; 8/13 (61.5%) improved, and 3/13 (23.1%) remained stable, suggesting an efficacy of these treatments. 

 

 

 Conclusions 

 AGO-Abs might be potential biomarkers of autoimmunity in patients with central and peripheral nonparaneoplastic neurologic diseases. In 7 patients, AGO-Abs were the only biomarkers; thus, their identification may be useful to suspect the autoimmune character of the neurologic disorder. 

 

 

 Classification of Evidence 

 This study provides Class III evidence that AGO-Abs are more frequent in patients with autoimmune neurologic diseases than controls.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{edel_extracellular_2021,

title = {Extracellular riboflavin induces anaerobic biofilm formation in Shewanella oneidensis},

author = {Miriam Edel and Gunnar Sturm and Katrin Sturm-Richter and Michael Wagner and Julia Novion Ducassou and Yohann Couté and Harald Horn and Johannes Gescher},

url = {https://biotechnologyforbiofuels.biomedcentral.com/articles/10.1186/s13068-021-01981-3},

doi = {10.1186/s13068-021-01981-3},

issn = {1754-6834},

year  = {2021},

date = {2021-06-01},

urldate = {2021-06-01},

journal = {Biotechnology for Biofuels},

volume = {14},

number = {1},

pages = {130},

abstract = {Abstract 

 

 Background 

 Some microorganisms can respire with extracellular electron acceptors using an extended electron transport chain to the cell surface. This process can be applied in bioelectrochemical systems in which the organisms produce an electrical current by respiring with an anode as electron acceptor. These organisms apply flavin molecules as cofactors to facilitate one-electron transfer catalyzed by the terminal reductases and in some cases as endogenous electron shuttles. 

 

 

 Results 

 

 In the model organism 

 Shewanella oneidensis 

 , riboflavin production and excretion trigger a specific biofilm formation response that is initiated at a specific threshold concentration, similar to canonical quorum-sensing molecules. Riboflavin-mediated messaging is based on the overexpression of the gene encoding the putrescine decarboxylase 

 speC 

 which leads to posttranscriptional overproduction of proteins involved in biofilm formation. Using a model of growth-dependent riboflavin production under batch and biofilm growth conditions, the number of cells necessary to produce the threshold concentration per time was deduced. Furthermore, our results indicate that specific retention of riboflavin in the biofilm matrix leads to localized concentrations, which by far exceed the necessary threshold value. 

 

 

 

 Conclusion 

 

 This study describes a new quorum-sensing mechanism in 

 S. oneidensis 

 . Biofilm formation of 

 S. oneidensis 

 is induced by low concentrations of riboflavin resulting in an upregulation of the ornithine-decarboxylase 

 speC 

 . The results can be applied for the development of strains catalyzing increased current densities in bioelectrochemical systems.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{alfaro_emerging_2021,

title = {The emerging landscape of single-molecule protein sequencing technologies},

author = {Javier Antonio Alfaro and Peggy Bohländer and Mingjie Dai and Mike Filius and Cecil J. Howard and Xander F. Kooten and Shilo Ohayon and Adam Pomorski and Sonja Schmid and Aleksei Aksimentiev and Eric V. Anslyn and Georges Bedran and Chan Cao and Mauro Chinappi and Etienne Coyaud and Cees Dekker and Gunnar Dittmar and Nicholas Drachman and Rienk Eelkema and David Goodlett and Sébastien Hentz and Umesh Kalathiya and Neil L. Kelleher and Ryan T. Kelly and Zvi Kelman and Sung Hyun Kim and Bernhard Kuster and David Rodriguez-Larrea and Stuart Lindsay and Giovanni Maglia and Edward M. Marcotte and John P. Marino and Christophe Masselon and Michael Mayer and Patroklos Samaras and Kumar Sarthak and Lusia Sepiashvili and Derek Stein and Meni Wanunu and Mathias Wilhelm and Peng Yin and Amit Meller and Chirlmin Joo},

url = {http://www.nature.com/articles/s41592-021-01143-1},

doi = {10.1038/s41592-021-01143-1},

issn = {1548-7091, 1548-7105},

year  = {2021},

date = {2021-06-01},

urldate = {2021-06-01},

journal = {Nature Methods},

volume = {18},

number = {6},

pages = {604--617},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{humbert_apoptotic_2021,

title = {Apoptotic mesenchymal stromal cells support osteoclastogenesis while inhibiting multinucleated giant cells formation in vitro},

author = {Paul Humbert and Meadhbh Á. Brennan and Julien De Lima and Régis Brion and Annie Adrait and Céline Charrier and Bénédicte Brulin and Valérie Trichet and Yohann Couté and Frédéric Blanchard and Pierre Layrolle},

url = {http://www.nature.com/articles/s41598-021-91258-4},

doi = {10.1038/s41598-021-91258-4},

issn = {2045-2322},

year  = {2021},

date = {2021-06-01},

urldate = {2021-06-01},

journal = {Scientific Reports},

volume = {11},

number = {1},

pages = {12144},

abstract = {Abstract 

 In bone regeneration induced by the combination of mesenchymal stromal cells (MSCs) and calcium-phosphate (CaP) materials, osteoclasts emerge as a pivotal cell linking inflammation and bone formation. Favorable outcomes are observed despite short-term engraftments of implanted MSCs, highlighting their major paracrine function and the possible implication of cell death in modulating their secretions. In this work, we focused on the communication from MSCs towards osteoclasts-like cells in vitro. MSCs seeded on a CaP biomaterial or undergoing induced apoptosis produced a conditioned media favoring the development of osteoclasts from human CD14+ monocytes. On the contrary, MSCs’ apoptotic secretion inhibited the development of inflammatory multinucleated giant cells formed after IL-4 stimulation. Components of MSCs’ secretome before and after apoptotic stress were compared using mass spectrometry-based quantitative proteomics and a complementary immunoassay for major cytokines. CXCR-1 and CXCR-2 ligands, primarily IL-8/CXCL-8 but also the growth-regulated proteins CXCL-1, -2 or -3, were suggested as the major players of MSCs’ pro-osteoclastic effect. These findings support the hypothesis that osteoclasts are key players in bone regeneration and suggest that apoptosis plays an important role in MSCs’ effectiveness.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pipier_constrained_2021,

title = {Constrained G4 structures unveil topology specificity of known and new G4 binding proteins},

author = {A. Pipier and A. Devaux and T. Lavergne and A. Adrait and Y. Couté and S. Britton and P. Calsou and J. F. Riou and E. Defrancq and D. Gomez},

url = {https://www.nature.com/articles/s41598-021-92806-8},

doi = {10.1038/s41598-021-92806-8},

issn = {2045-2322},

year  = {2021},

date = {2021-06-01},

urldate = {2021-06-01},

journal = {Scientific Reports},

volume = {11},

number = {1},

pages = {13469},

abstract = {G-quadruplexes (G4) are non-canonical secondary structures consisting in stacked tetrads of hydrogen-bonded guanines bases. An essential feature of G4 is their intrinsic polymorphic nature, which is characterized by the equilibrium between several conformations (also called topologies) and the presence of different types of loops with variable lengths. In cells, G4 functions rely on protein or enzymatic factors that recognize and promote or resolve these structures. In order to characterize new G4-dependent mechanisms, extensive researches aimed at identifying new G4 binding proteins. Using G-rich single-stranded oligonucleotides that adopt non-controlled G4 conformations, a large number of G4-binding proteins have been identified in vitro, but their specificity towards G4 topology remained unknown. Constrained G4 structures are biomolecular objects based on the use of a rigid cyclic peptide scaffold as a template for directing the intramolecular assembly of the anchored oligonucleotides into a single and stabilized G4 topology. Here, using various constrained RNA or DNA G4 as baits in human cell extracts, we establish the topology preference of several well-known G4-interacting factors. Moreover, we identify new G4-interacting proteins such as the NELF complex involved in the RNA-Pol II pausing mechanism, and we show that it impacts the clastogenic effect of the G4-ligand pyridostatin.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{montillet_plastidial_2021,

title = {Plastidial and cytosolic thiol reductases participate in the control of stomatal functioning},

author = {Jean-Luc Montillet and Damien Rondet and Sabine Brugière and Patricia Henri and Dominique Rumeau and Jean-Philippe Reichheld and Yohann Couté and Nathalie Leonhardt and Pascal Rey},

doi = {10.1111/pce.14013},

issn = {1365-3040},

year  = {2021},

date = {2021-05-01},

urldate = {2021-05-01},

journal = {Plant, Cell & Environment},

volume = {44},

number = {5},

pages = {1417--1435},

abstract = {Stomatal movements via the control of gas exchanges determine plant growth in relation to environmental stimuli through a complex signalling network involving reactive oxygen species that lead to post-translational modifications of Cys and Met residues, and alter protein activity and/or conformation. Thiol-reductases (TRs), which include thioredoxins, glutaredoxins (GRXs) and peroxiredoxins (PRXs), participate in signalling pathways through the control of Cys redox status in client proteins. Their involvement in stomatal functioning remains poorly characterized. By performing a mass spectrometry-based proteomic analysis, we show that numerous thiol reductases, like PRXs, are highly abundant in guard cells. When investigating various Arabidopsis mutants impaired in the expression of TR genes, no change in stomatal density and index was noticed. In optimal growth conditions, a line deficient in cytosolic NADPH-thioredoxin reductases displayed higher stomatal conductance and lower leaf temperature evaluated by thermal infrared imaging. In contrast, lines deficient in plastidial 2-CysPRXs or type-II GRXs exhibited compared to WT reduced conductance and warmer leaves in optimal conditions, and enhanced stomatal closure in epidermal peels treated with abscisic acid or hydrogen peroxide. Altogether, these data strongly support the contribution of thiol redox switches within the signalling network regulating guard cell movements and stomatal functioning.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{chiari_leafy_2021,

title = {LEAFY protein crystals with a honeycomb structure as a platform for selective preparation of outstanding stable bio-hybrid materials},

author = {Lucile Chiari and Philippe Carpentier and Sylvie Kieffer-Jaquinod and Alice Gogny and Julien Perard and Stéphane Ravanel and David Cobessi and Stéphane Ménage and Renaud Dumas and Olivier Hamelin},

doi = {10.1039/d1nr00268f},

issn = {2040-3372},

year  = {2021},

date = {2021-05-01},

urldate = {2021-05-01},

journal = {Nanoscale},

abstract = {Well-organized protein assemblies offer many properties that justify their use for the design of innovative bionanomaterials. Herein, crystals of the oligomerization domain of the LEAFY protein from Ginkgo biloba, organized in a honeycomb architecture, were used as a modular platform for the selective grafting of a ruthenium-based complex. The resulting bio-hybrid crystalline material was fully characterized by UV-visible and Raman spectroscopy and by mass spectrometry and LC-MS analysis after selective enzymatic digestion. Interestingly, insertion of complexes within the tubular structure affords an impressive increase in stability of the crystals, eluding the use of stabilizing cross-linking strategies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pallavicini_goldberg-shprintzen_2021,

title = {Goldberg-Shprintzen syndrome protein KIF1BP is a CITK interactor implicated in cytokinesis.},

author = {Gianmarco Pallavicini and Marta Gai and Giorgia Iegiani and Gaia Elena Berto and Annie Adrait and Yohann Couté and Ferdinando Di Cunto},

url = {https://doi.org/10.1242/jcs.250902},

doi = {10.1242/jcs.250902},

issn = {0021-9533},

year  = {2021},

date = {2021-05-01},

urldate = {2021-05-01},

journal = {Journal of Cell Science},

number = {jcs.250902},

abstract = {Goldberg-Shprintzen disease (GOSHS) is a rare microcephaly syndrome accompanied by intellectual disability, dysmorphic facial features, peripheral neuropathy and Hirschsprung disease. It is associated with recessive mutations in the gene encoding kinesin family member 1-binding protein (KIF1BP). The encoded protein regulates axon microtubules dynamics, kinesin attachment and mitochondrial biogenesis, but it is not clear how its loss could lead to microcephaly. We identified KIF1BP in the interactome of Citron Kinase (CITK), a protein produced by primary hereditary microcephaly 17 (MCPH17) gene. KIF1BP and CITK interact under physiological conditions in mitotic cells. Similar to CITK, KIF1BP is enriched at the midbody ring and is required for cytokinesis. The association between KIF1BP and CITK can be influenced by CITK activity and the two proteins may antagonize each other for their midbody localization. KIF1BP knockdown decreases microtubule stability, increases KIF23 midbody levels and impairs midbody localization of KIF14, as well as of Chromosome Passenger Complex. These data indicate that KIF1BP is a CITK interactor involved in midbody maturation and abscission and suggest that cytokinesis failure may contribute to the microcephaly phenotype observed in GOSHS.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{schmid_developing_2021,

title = {Developing Rhodobacter sphaeroides for cathodic biopolymer production},

author = {Ferdinand Schmid and Julia Novion Ducassou and Yohann Couté and Johannes Gescher},

url = {https://linkinghub.elsevier.com/retrieve/pii/S0960852421006805},

doi = {10.1016/j.biortech.2021.125340},

issn = {09608524},

year  = {2021},

date = {2021-05-01},

urldate = {2021-05-01},

journal = {Bioresource Technology},

pages = {125340},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{hseiky_small_2021,

title = {Small Mass but Strong Information: Diagnostic Ions Provide Crucial Clues to Correctly Identify Histone Lysine Modifications},

author = {Alaa Hseiky and Marion Crespo and Sylvie Kieffer-Jaquinod and François Fenaille and Delphine Pflieger},

doi = {10.3390/proteomes9020018},

issn = {2227-7382},

year  = {2021},

date = {2021-04-01},

urldate = {2021-04-01},

journal = {Proteomes},

volume = {9},

number = {2},

abstract = {(1) Background: The proteomic analysis of histones constitutes a delicate task due to the combination of two factors: slight variations in the amino acid sequences of variants and the multiplicity of post-translational modifications (PTMs), particularly those occurring on lysine residues. (2) Methods: To dissect the relationship between both aspects, we carefully evaluated PTM identification on lysine 27 from histone H3 (H3K27) and the artefactual chemical modifications that may lead to erroneous PTM determination. H3K27 is a particularly interesting example because it can bear a range of PTMs and it sits nearby residues 29 and 31 that vary between H3 sequence variants. We discuss how the retention times, neutral losses and immonium/diagnostic ions observed in the MS/MS spectra of peptides bearing modified lysines detectable in the low-mass region might help validate the identification of modified sequences. (3) Results: Diagnostic ions carry key information, thereby avoiding potential mis-identifications due to either isobaric PTM combinations or isobaric amino acid-PTM combinations. This also includes cases where chemical formylation or acetylation of peptide N-termini artefactually occurs during sample processing or simply in the timeframe of LC-MS/MS analysis. Finally, in the very subtle case of positional isomers possibly corresponding to a given mass of lysine modification, the immonium and diagnostic ions may allow the identification of the in vivo structure.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{curien_mixotrophic_2021,

title = {Mixotrophic growth of the extremophile Galdieria sulphuraria reveals the flexibility of its carbon assimilation metabolism},

author = {Gilles Curien and Dagmar Lyska and Erika Guglielmino and Phillip Westhoff and Janina Janetzko and Marianne Tardif and Clément Hallopeau and Sabine Brugière and Davide Dal Bo and Johan Decelle and Benoit Gallet and Denis Falconet and Michele Carone and Claire Remacle and Myriam Ferro and Andreas P. M. Weber and Giovanni Finazzi},

doi = {10.1111/nph.17359},

issn = {1469-8137},

year  = {2021},

date = {2021-03-01},

urldate = {2021-03-01},

journal = {The New Phytologist},

abstract = {Galdieria sulphuraria is a cosmopolitan microalga found in volcanic hot springs and calderas. It grows at low pH in photoautotrophic (use of light as a source of energy) or heterotrophic (respiration as a source of energy) conditions, using an unusually broad range of organic carbon sources. Previous data suggested that G. sulphuraria cannot grow mixotrophically (simultaneously exploiting light and organic carbon as energy sources), its photosynthetic machinery being repressed by organic carbon. Here, we show that G. sulphuraria SAG21.92 thrives in photoautotrophy, heterotrophy and mixotrophy. By comparing growth, biomass production, photosynthetic and respiratory performances in these three trophic modes, we show that addition of organic carbon to cultures (mixotrophy) relieves inorganic carbon limitation of photosynthesis thanks to increased CO2 supply through respiration. This synergistic effect is lost when inorganic carbon limitation is artificially overcome by saturating photosynthesis with added external CO2 . Proteomic and metabolic profiling corroborates this conclusion suggesting that mixotrophy is an opportunistic mechanism to increase intracellular CO2 concentration under physiological conditions, boosting photosynthesis by enhancing the carboxylation activity of Ribulose-1,5-bisphosphate carboxylase-oxygenase (Rubisco) and decreasing photorespiration. We discuss possible implications of these findings for the ecological success of Galdieria in extreme environments and for biotechnological applications.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{borges_well_2021,

title = {Well Plate Maker: A user-friendly randomized block design application to limit batch effects in largescale biomedical studies},

author = {Hélène Borges and Anne-Marie Hesse and Alexandra Kraut and Yohann Couté and Virginie Brun and Thomas Burger},

doi = {10.1093/bioinformatics/btab065},

issn = {1367-4811},

year  = {2021},

date = {2021-02-01},

urldate = {2021-02-01},

journal = {Bioinformatics (Oxford, England)},

abstract = {SUMMARY: Many factors can influence results in clinical research, in particular bias in the distribution of samples prior to biochemical preparation. Well Plate Maker is a user-friendly application to design single- or multiple-well plate assays. It allows multiple group experiments to be randomized and therefore helps to reduce possible batch effects. Although primarily fathered to optimize the design of clinical sample analysis by high throughput mass spectrometry (e.g. proteomics or metabolomics), it includes multiple options to limit edge-of-plate effects, to incorporate control samples, or to limit cross-contamination. It thus fits the constraints of many experimental fields. 

AVAILABILITY AND IMPLEMENTATION: Well Plate Maker is implemented in R and available at Bioconductor repository (https://bioconductor.org/packages/wpm) under the open source Artistic 2.0 license. In addition to classical scripting, it can be used through a graphical user interface, developed with Shiny technology. 

SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{permiakova_chickn_2021,

title = {CHICKN: extraction of peptide chromatographic elution profiles from large scale mass spectrometry data by means of Wasserstein compressive hierarchical cluster analysis},

author = {Olga Permiakova and Romain Guibert and Alexandra Kraut and Thomas Fortin and Anne-Marie Hesse and Thomas Burger},

doi = {10.1186/s12859-021-03969-0},

issn = {1471-2105},

year  = {2021},

date = {2021-02-01},

urldate = {2021-02-01},

journal = {BMC bioinformatics},

volume = {22},

number = {1},

pages = {68},

abstract = {BACKGROUND: The clustering of data produced by liquid chromatography coupled to mass spectrometry analyses (LC-MS data) has recently gained interest to extract meaningful chemical or biological patterns. However, recent instrumental pipelines deliver data which size, dimensionality and expected number of clusters are too large to be processed by classical machine learning algorithms, so that most of the state-of-the-art relies on single pass linkage-based algorithms. 

RESULTS: We propose a clustering algorithm that solves the powerful but computationally demanding kernel k-means objective function in a scalable way. As a result, it can process LC-MS data in an acceptable time on a multicore machine. To do so, we combine three essential features: a compressive data representation, Nyström approximation and a hierarchical strategy. In addition, we propose new kernels based on optimal transport, which interprets as intuitive similarity measures between chromatographic elution profiles. 

CONCLUSIONS: Our method, referred to as CHICKN, is evaluated on proteomics data produced in our lab, as well as on benchmark data coming from the literature. From a computational viewpoint, it is particularly efficient on raw LC-MS data. From a data analysis viewpoint, it provides clusters which differ from those resulting from state-of-the-art methods, while achieving similar performances. This highlights the complementarity of differently principle algorithms to extract the best from complex LC-MS data.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{harrer_production_2021,

title = {Production of acetoin from renewable resources under heterotrophic and mixotrophic conditions},

author = {Daniel Härrer and Carina Windhorst and Nicola Böhner and Julia Novion Ducassou and Yohann Couté and Johannes Gescher},

url = {https://linkinghub.elsevier.com/retrieve/pii/S0960852421002054},

doi = {10.1016/j.biortech.2021.124866},

issn = {09608524},

year  = {2021},

date = {2021-02-01},

urldate = {2021-02-01},

journal = {Bioresource Technology},

pages = {124866},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{vellino_cross-talk_2021,

title = {Cross-talk between the calcium channel TRPV4 and reactive oxygen species interlocks adhesive and degradative functions of invadosomes},

author = {Sanela Vellino and Christiane Oddou and Paul Rivier and Cyril Boyault and Edwige Hiriart-Bryant and Alexandra Kraut and René Martin and Yohann Couté and Hans-Joachim Knölker and Miguel A. Valverde and Corinne Albigès-Rizo and Olivier Destaing},

url = {https://rupress.org/jcb/article/doi/10.1083/jcb.201910079/211651/Cross-talk-between-the-calcium-channel-TRPV4-and},

doi = {10.1083/jcb.201910079},

issn = {0021-9525, 1540-8140},

year  = {2021},

date = {2021-02-01},

urldate = {2021-02-01},

journal = {Journal of Cell Biology},

volume = {220},

number = {2},

pages = {e201910079},

abstract = {Invadosomes support cell invasion by coupling both acto-adhesive and extracellular matrix degradative functions, which are apparently antagonistic. β1-integrin dynamics regulate this coupling, but the actual sensing mechanism and effectors involved have not yet been elucidated. Using genetic and reverse genetic approaches combined with biochemical and imaging techniques, we now show that the calcium channel TRPV4 colocalizes with β1-integrins at the invadosome periphery and regulates its activation and the coupling of acto-adhesive and degradative functions. TRPV4-mediated regulation of podosome function depends on its ability to sense reactive oxygen species (ROS) in invadosomes’ microenvironment and involves activation of the ROS/calcium-sensitive kinase Ask1 and binding of the motor MYO1C. Furthermore, disease-associated TRPV4 gain-of-function mutations that modulate ECM degradation are also implicated in the ROS response, which provides new perspectives in our understanding of the pathophysiology of TRPV4 channelopathies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{707,

title = {Mapping rRNA 2'-O-methylations and identification of C/D snoRNAs in Arabidopsis thaliana plants},

author = {J Azevedo-Favory and C Gaspin and L Ayadi and C Montacie and V Marchand and E Jobet and M Rompais and C Carapito and Y Motorin and J Saez-Vasquez},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33596769},

doi = {10.1080/15476286.2020.1869892},

issn = {1555-8584 (Electronic) 1547-6286 (Linking)},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {RNA Biol},

pages = {1-18},

abstract = {In all eukaryotic cells, the most abundant modification of ribosomal RNA (rRNA) is methylation at the ribose moiety (2'-O-methylation). Ribose methylation at specific rRNA sites is guided by small nucleolar RNAs (snoRNAs) of C/D-box type (C/D snoRNA) and achieved by the methyltransferase Fibrillarin (FIB). Here we used the Illumina-based RiboMethSeq approach for mapping rRNA 2'-O-methylation sites in A. thaliana Col-0 (WT) plants. This analysis detected novel C/D snoRNA-guided rRNA 2'-O-methylation positions and also some orphan sites without a matching C/D snoRNA. Furthermore, immunoprecipitation of Arabidopsis FIB2 identified and demonstrated expression of C/D snoRNAs corresponding to majority of mapped rRNA sites. On the other hand, we show that disruption of Arabidopsis Nucleolin 1 gene (NUC1), encoding a major nucleolar protein, decreases 2'-O-methylation at specific rRNA sites suggesting functional/structural interconnections of 2'-O-methylation with nucleolus organization and plant development. Finally, based on our findings and existent database sets, we introduce a new nomenclature system for C/D snoRNA in Arabidopsis plants.},

note = {Azevedo-Favory, J 

Gaspin, C 

Ayadi, L 

Montacie, C 

Marchand, V 

Jobet, E 

Rompais, M 

Carapito, C 

Motorin, Y 

Saez-Vasquez, J 

eng 

2021/02/19 06:00 

RNA Biol. 2021 Feb 17:1-18. doi: 10.1080/15476286.2020.1869892.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}