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@article{TeletcheaTNF2025,

title = {Molecular determinants of TNFR1:TNFα binding and dynamics in a physiological membrane environment},

author = {Elena Álvarez-Sánchez and Simon Huet and Stéphane Téletchéa},

editor = {Elsevier},

doi = {10.1016/j.crstbi.2025.100177},

year  = {2026},

date = {2026-06-01},

urldate = {2025-12-18},

journal = {Current Research in Structural Biology},

volume = {26},

pages = {100177},

abstract = {Tumor Necrosis Factor alpha (TNFα) is a pro-inflammatory cytokine critical for regulating cell survival and death. Under pathological conditions, excessive TNFα activity can lead to chronic inflammation, contributing to diseases such as inflammatory bowel disease and other autoimmune disorders. While structural studies have elucidated the atomistic details of TNFα binding to its receptor, TNF Receptor 1 (TNFR1), the influence of the membrane environment on this interaction remains poorly characterized experimentally. In this study, we employed advanced all-atom Gaussian accelerated molecular dynamics simulations to investigate how lipid-mediated interactions modulate the TNFα–TNFR1 complex. We identified key residues on both the cytokine and its receptor that govern trimer assembly, receptor binding, and potential pathological alterations. Our analysis confirmed previously identified functional sites and revealed new residues likely to contribute to the structural stability and dynamics of the complex. These findings provide a more comprehensive understanding of the molecular determinants of TNF signaling and offer a foundation for future experimental investigations into the receptor-ligand interface and membrane-mediated regulation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Mahoudeau2026,

title = {The interplay between the marine diazotroph                    \textit{Vibrio diazotrophicus}                    and its prophage shapes both biofilm structure and nitrogen release},

author = {Louise Mahoudeau and Pauline Crétin and Aurélie Joublin-Delavat and Sophie Rodrigues and Clara Guillouche and Isabelle Louvet and Nadège Bienvenu and Claire Geslin and Gabriel Dulaquais and Jean-François Maguer and François Delavat},

editor = {Julia C. van Kessel},

doi = {10.1128/aem.01564-25},

issn = {1098-5336},

year  = {2026},

date = {2026-01-27},

urldate = {2026-01-27},

journal = {Appl Environ Microbiol},

volume = {92},

number = {1},

publisher = {American Society for Microbiology},

abstract = {<jats:title>ABSTRACT</jats:title>

                  <jats:sec>

                    <jats:title/>

                    <jats:p>

                      Marine environments are frequently oligotrophic, characterized by low amount of bioassimilable nitrogen sources. At the global scale, the microbial fixation of N₂, or diazotrophy, represents the primary source of fixed nitrogen in pelagic marine ecosystems, playing a key role in supporting primary production and driving the export of organic matter to the deep ocean. However, given the high energetic cost of N₂ fixation, the active release of fixed nitrogen by diazotrophs appears counterintuitive, suggesting the existence of alternative passive release pathways that remain understudied to date. Here, we show that the marine non-cyanobacterial diazotroph

                      <jats:italic toggle="yes">Vibrio diazotrophicus</jats:italic>

                      is endowed with a prophage belonging to the

                      <jats:italic toggle="yes">Myoviridae</jats:italic>

                      family, whose expression is induced under anoxic and biofilm-forming conditions. We demonstrate that this prophage can spontaneously excise from the genome of its host and that it forms intact and infective phage particles. Moreover, phage-mediated host cell lysis leads to increased biofilm production compared with a prophage-free derivative mutant and to increased release of dissolved organic carbon and ammonium. Altogether, the results suggest that viruses may play a previously unrecognized role in oceanic ecosystem dynamics by structuring microhabitats suitable for diazotrophy and by contributing to the recycling of (in)organic matter.

                    </jats:p>

                  </jats:sec>

                  <jats:sec>

                    <jats:title>IMPORTANCE</jats:title>

                    <jats:p>

                      Diazotrophs are key players in ocean functioning by providing fixed nitrogen to ecosystems and fueling primary production. However, from a physiological point of view, the active release of nitrogenous compounds by diazotrophs is paradoxical, since they would invest in an energy-intensive process and supply nutrient to non-sibling cells, with the risk of being outcompeted. Therefore, alternative ways leading to the release of fixed nitrogen must exist. Here, we show that the marine non-cyanobacterial diazotroph

                      <jats:italic toggle="yes">Vibrio diazotrophicus</jats:italic>

                      possesses one prophage, whose activation leads to cell death, increased biofilm production, and the release of dissolved organic compounds and ammonium. Taken together, our results provide evidence that marine phage–diazotroph interplay leads to the creation of microhabitats suitable for diazotrophy, such as biofilm, and to nutrient cycling, and contributes to better understanding of the role of viruses in marine ecosystems.

                    </jats:p>

                  </jats:sec>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{TeletcheaSac7d2025,

title = {Energetics Decomposition of Sac7d:DNA Decrypts Amino Acids Role Without DNA Sequence Selectivity},

author = {Elena Álvarez-Sánchez and Bernard Offmann and Simon Huet and Stéphane Téletchéa},

editor = {Wiley},

doi = {10.1002/jmr.70021},

year  = {2026},

date = {2026-01-05},

urldate = {2025-12-15},

journal = {Journal Of Molecular Recognition},

volume = {39},

issue = {1},

pages = {e70021},

abstract = {Sac7d is a 7 kDa protein belonging to the class of the small chromosomal proteins from archeon Sulfolobus acidocaldarius. Sac7d was discovered in 1974 in Yellowstone National Parks geysers, and studied extensively since then for its remarkable stability at large pH and temperature ranges. Sac7d binds to the DNA minor groove, thereby protecting the host genome from extreme conditions by increasing the DNA melting temperature. In this study, we analyzed the Sac7d-DNA complex using 1 μs molecular dynamics simulations. The interaction energy of the interface was decomposed using Molecular Mechanics with Generalized Born Surface Area (MM/GBSA) to determine the residues that contributed most significantly to DNA binding. Out of 12 amino acids considered essential for DNA binding, three were newly identified in this study and had not been previously reported. One of these new amino acids, R63, may be involved in a dynamic protein-DNA interaction. The simulations performed also revealed a sliding motion of Sac7d over double-stranded DNA, suggesting a minimal sequence dependence interaction. Our analysis thus provides novel insights into how the Sac7d chaperones allow to protect DNA from degradation in extreme conditions. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Gamage2026,

title = {Co-culturing with bacteria modulates fatty acid composition in benthic diatom biofilms for lipid-based biotechnologies: A case study of Amphora sp.},

author = {Nadeeshani Dehel Gamage and Aurélie Mossion and Paul Déléris and François Delavat and Leïla Tirichine and Vony Rabesaotra and Thierry Lebeau and Gaëtane Wielgosz-Collin and Vona Méléder},

doi = {10.1016/j.algal.2025.104449},

issn = {2211-9264},

year  = {2026},

date = {2026-01-00},

urldate = {2026-01-00},

journal = {Algal Research},

volume = {93},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bull2025,

title = {Targeting metastasis in paediatric bone sarcomas},

author = {Emma C. Bull and Archana Singh and Amy M. Harden and Kirsty Soanes and Hala Habash and Lisa Toracchio and Marianna Carrabotta and Christina Schreck and Karan M. Shah and Paulina Velasco Riestra and Margaux Chantoiseau and Maria Eugénia Marques Da Costa and Gaël Moquin-Beaudry and Pan Pantziarka and Edidiong Akanimo Essiet and Craig Gerrand and Alison Gartland and Linda Bojmar and Anna Fahlgren and Antonin Marchais and Evgenia Papakonstantinou and Eleni M. Tomazou and Didier Surdez and Dominique Heymann and Florencia Cidre-Aranaz and Olivia Fromigue and Darren W. Sexton and Nikolas Herold and Thomas G. P. Grünewald and Katia Scotlandi and Michaela Nathrath and Darrell Green},

doi = {10.1186/s12943-025-02365-z},

issn = {1476-4598},

year  = {2025},

date = {2025-12-00},

urldate = {2025-12-00},

journal = {Mol Cancer},

volume = {24},

number = {1},

publisher = {Springer Science and Business Media LLC},

abstract = {<jats:title>Abstract</jats:title>

          <jats:p>Paediatric bone sarcomas (e.g. Ewing sarcoma, osteosarcoma) comprise significant biological and clinical heterogeneity. This extreme heterogeneity affects response to systemic therapy, facilitates inherent and acquired drug resistance and possibly underpins the origins of metastatic disease, a key component implicit in cancer related death. Across all cancers, metastatic models have offered competing accounts on when dissemination occurs, either early or late during tumorigenesis, whether metastases at different foci arise independently and directly from the primary tumour or give rise to each other, i.e. metastases-to-metastases dissemination, and whether cell exchange occurs between synchronously growing lesions. Although it is probable that all the above mechanisms can lead to metastatic disease, clinical observations indicate that distinct modes of metastasis might predominate in different cancers. Around 70% of patients with bone sarcoma experience metastasis during their disease course but the fundamental molecular and cell mechanisms underlying spread are equivocal. Newer therapies such as tyrosine kinase inhibitors have shown promise in reducing metastatic relapse in trials, nonetheless, not all patients respond and 5-year overall survival remains at ~ 50%. Better understanding of potential bone sarcoma biological subgroups, the role of the tumour immune microenvironment, factors that promote metastasis and clinical biomarkers of prognosis and drug response are required to make progress. In this review, we provide a comprehensive overview of the approaches to manage paediatric patients with metastatic Ewing sarcoma and osteosarcoma. We describe the molecular basis of the tumour immune microenvironment, cell plasticity, circulating tumour cells and the development of the pre-metastatic niche, all required for successful distant colonisation. Finally, we discuss ongoing and upcoming patient clinical trials, biomarkers and gene regulatory networks amenable to the development of anti-metastasis medicines.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}