5′ and 3′ ends of chloroplast transcripts can both be stabilised by protein ‘caps': a new model for polycistronic RNA maturation

International audienc

Light-driven processes: key players of the functional biodiversity in microalgae

International audienc

Epstein-Barr Virus and immune status imprint the immunogenomics of non-Hodgkin lymphomas occurring in immune-suppressed environments

Non-Hodgkin lymphomas (NHL) commonly occur in immune-deficient (ID) patients, both HIV-infected and transplanted, and are often EBV-driven with cerebral localization, raising the question of tumor immunogenicity, a critical issue for treatment responses. We investigated the immunogenomics of 68 lymphoproliferative disorders from 51 ID (34 posttransplant, 17 HIV+) and 17 immunocompetent patients. Overall, 72% were Large B Cells Lymphoma (LBCL) and 25% were primary central-nervous-system lymphoma (PCNSL) while 40% were EBV-positive. Tumor whole-exome and RNA sequencing, along with a bioinformatics pipeline allowed analysis of tumor mutational burden (TMB), tumor landscape and microenvironment (TME) and prediction of tumor neoepitopes. Both TMB (2.2 vs 3.4/Mb, p=0.001) and neoepitopes numbers (40 vs 200, p=0.00019) were lower in EBVpositive than in EBV-negative NHL, regardless of the immune status. In contrast both EBV and the immune status influenced the tumor mutational profile, with HNRNPF and STAT3 mutations exclusively observed in EBV-positive and ID NHL, respectively. Peripheral blood T-cell responses against tumor neoepitopes were detected in all EBV-negative cases but in only half EBV-positive ones, including responses against IgH-derived MHC-class-II restricted neoepitopes. The TME analysis showed higher CD8 T cell infiltrates in EBVpositive vs EBV-negative NHL, together with a more tolerogenic profile composed of Tregs, type-M2 macrophages and an increased expression of negative immune-regulators. Our results highlight that the immunogenomics of NHL in patients with immunodeficiency primarily relies on the tumor EBV status, while T cell recognition of tumor- and IgH-specific neoepitopes is conserved in EBV-negative patients, offering potential opportunities for future T cell-based immune therapies

Understanding the nervous system: Lessons from Frontiers in Neurophotonics

The Frontiers in Neurophotonics Symposium is a biennial event that brings together neurobiologists and physicists/engineers who share interest in the development of leading-edge photonics-based approaches to understand and manipulate the nervous system, from its individual molecular components to complex networks in the intact brain. In this Community paper, we highlight several topics that have been featured at the symposium that took place in October 2022 in Québec City, Canada

Le système d expression du gène chloroplastique petA chez Chlamydomonas reinhardtii

Depuis l endosymbiose ayant mené au chloroplaste de l algue verte unicellulaire Chlamydomonas reinhardtii, la plupart des gènes de l endosymbiote primitif ont été transférés dans le génome nucléaire de l hôte, qui code donc des sous-unités des complexes de l appareil photosynthétique, mais aussi des facteurs régulant l expression des gènes restés dans le chloroplaste. Le gène chloroplastique petA, codant le cytochrome f, possède deux facteurs spécifiques : MCA1 est responsable de la stabilisation de l ARNm petA, et TCA1 de l activation de sa traduction. D autre part, la synthèse du cytochrome f est réprimée quand celui-ci ne peut s assembler au sein du complexe b6f, par le contrôle par épistasie de synthèse (ou CES). Le mécanisme moléculaire permettant l expression du gène petA et son contrôle par le CES a été largement dévoilé grâce aux travaux présentés dans ce manuscrit : les facteurs MCA1 et TCA1 forment différents complexes de haut poids moléculaires, pouvant contenir l ARNm petA, et le cytochrome f non assemblé signalise la dégradation de MCA1 par les protéases FtsH et ClpP.Par ailleurs, ces travaux ont fortuitement mené à la découverte d une mutation nucléaire dominante, su0, conduisant à la dégradation de l ARNm petA, mais seulement lors de sa traduction. La mutation causant ce phénotype intriguant, indépendante des facteurs MCA1 et TCA1 et du CES, a été localisée dans une région de 300 kb sur le chromosome 15, mais n a pas encore été identifiée.PARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF