دورية أكاديمية

Loss of NR5A1 in mouse Sertoli cells after sex determination changes cellular identity and induces cell-death by anoikis

التفاصيل البيبلوغرافية
العنوان: Loss of NR5A1 in mouse Sertoli cells after sex determination changes cellular identity and induces cell-death by anoikis
المؤلفون: Souali-Crespo, Sirine, Condrea, Diana, Vernet, Nadège, Feret, Betty, Klopfenstein, Muriel, Grandgirard, Erwan, Alunni, Violaine, Cerciat, Marie, Jung, Matthieu, Mayère, Chloé, Nef, Serge, Mark, Manuel, Chalmel, Frédéric, Ghyselinck, Norbert B
المساهمون: Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hôpitaux universitaires de Genève = University Hospitals of Geneva (HUG), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique EHESP (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), École des Hautes Études en Santé Publique EHESP (EHESP), This work was supported by Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale and Université de Strasbourg. It was also supported by grants from Fondation pour la Recherche Médicale (FRM FDT201904008001), Agence Nationale de la Recherche (ANR-16-CE14-0017, ARESSERC project), and in part by the grant ANR-10-LABX-0030-INRT, a French State fund managed by the Agence Nationale de la Recherche under the frame Programme Investissements d'Avenir labelled ANR-10-IDEX-0002-02. Open Access funding provided by Agence Nationale de la Recherche. Deposited in PMC for immediate release., ANR-16-CE14-0017,ARESSERC,DECOUVRIR LES VOIES NON-CANONIQUES DE SIGNALISATION RELAYEES PAR L'ACIDE RETINOÏQUE IN VIVO: LA CELLULE DE SERTOLI COMME MODELE D'ETUDE(2016), ANR-10-LABX-0030,INRT,Integrative Biology : Nuclear dynamics- Regenerative medicine - Translational medicine(2010), ANR-10-IDEX-0002,UNISTRA,Par-delà les frontières, l'Université de Strasbourg(2010)
المصدر: ISSN: 0950-1991.
بيانات النشر: HAL CCSD
Company of Biologists
سنة النشر: 2023
المجموعة: Université de Rennes 1: Publications scientifiques (HAL)
مصطلحات موضوعية: Gonad, Integrin, Leydig, Mutant, SF-1, Testis, [SDV.BDD.EO]Life Sciences [q-bio]/Development Biology/Embryology and Organogenesis, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN]
الوصف: International audience ; To investigate the role of the nuclear receptor NR5A1 in testis after sex determination, we have analyzed mice lacking NR5A1 in Sertoli cells (SC) from embryonic day (E) 13.5 onwards. Ablation of Nr5a1 impairs the expression of genes characteristic of the SC identity (e.g., Sox9, Amh), causes SC death from E14.5 through a Trp53-independent mechanism related to anoikis, and induces disorganization of the testis cords. Together, these effects cause germ cells to enter meiosis and die. Single-cell RNA-sequencing experiments revealed that NR5A1-deficient SC change their molecular identity: some acquire a "pre-granulosa-like" identity, while other revert to a "supporting progenitor-like" cell identity, most of them being "intersex" because they express both testicular and ovarian genes. Fetal Leydig cells (LC) do not display significant changes, indicating that SC are not required beyond E14.5 for their emergence or maintenance. In contrast, adult LC were absent from the postnatal testes. In addition, adult mutant males display persistence of Müllerian duct derivatives, decreased anogenital distance and reduced penis length, which can be explained by the loss of AMH and testosterone synthesis due to SC failure.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/38063846; hal-04341919; https://hal.science/hal-04341919Test; https://hal.science/hal-04341919/documentTest; https://hal.science/hal-04341919/file/dev201710.pdfTest; PUBMED: 38063846
DOI: 10.1242/dev.201710
الإتاحة: https://doi.org/10.1242/dev.201710Test
https://hal.science/hal-04341919Test
https://hal.science/hal-04341919/documentTest
https://hal.science/hal-04341919/file/dev201710.pdfTest
حقوق: http://creativecommons.org/licenses/byTest/ ; info:eu-repo/semantics/OpenAccess
رقم الانضمام: edsbas.11A528D1
قاعدة البيانات: BASE