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<datestamp>2017-12-21</datestamp>
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<title lang=en>DICER Regulates the Formation and Maintenance of Cell-Cell Junctions in the Mouse Seminiferous Epithelium</title>
<creator>Korhonen, Hanna Maria</creator>
<creator>Yadav, Ram Prakash</creator>
<creator>Da Ros, Matteo</creator>
<creator>Chalmel, Frédéric</creator>
<creator>Zimmermann, Céline</creator>
<creator>Toppari, Jorma</creator>
<creator>Nef, Serge</creator>
<creator>Kotaja, Noora</creator>
<contributor>University of Turku</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - 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 )</contributor>
<contributor>Department of Genetic Medicine and Development ; University of Geneva Medical School</contributor>
<contributor>Institute of Biomedicine/Physiology ; Institute of Biomedicine/Physiology</contributor>
<contributor>Virus, Environnement et Reproduction ; Groupe d'Etude de la Reproduction Chez l'Homme et les Mammiferes (GERHM) ; Université de Rennes 1 (UR1) - IFR140 - Institut National de la Santé et de la Recherche Médicale (INSERM) - Université de Rennes 1 (UR1) - IFR140 - Institut National de la Santé et de la Recherche Médicale (INSERM) - Department of Genetic Medicine and Development ; University of Geneva Medical School - University of Geneva Medical School</contributor>
<description>International audience</description>
<source>ISSN: 0006-3363</source>
<source>EISSN: 1529-7268</source>
<source>Biology of Reproduction</source>
<publisher>Society for the Study of Reproduction</publisher>
<identifier>hal-01274239</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01274239</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01274239</source>
<source>Biology of Reproduction, Society for the Study of Reproduction, 2015, 93 (6), pp.139. 〈10.1095/biolreprod.115.131938〉</source>
<identifier>DOI : 10.1095/biolreprod.115.131938</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1095/biolreprod.115.131938</relation>
<identifier>PUBMED : 26510868</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26510868</relation>
<language>en</language>
<subject lang=en>apical ectoplasmic specialization</subject>
<subject lang=en> blood-testis barrier</subject>
<subject lang=en> cell-cell junction</subject>
<subject lang=en> DICER</subject>
<subject lang=en> gene regulation</subject>
<subject lang=en> miRNA</subject>
<subject lang=en> Spermatogenesis</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>The endonuclease DICER that processes micro-RNAs and small interfering RNAs is essential for normal spermatogenesis and male fertility. We previously showed that the deletion of Dicer1 gene in postnatal spermatogonia in mice using Ngn3 promoter-driven Cre expression caused severe defects in the morphogenesis of haploid spermatid to mature spermatozoon, including problems in cell polarization and nuclear elongation. In this study, we further analyzed the same mouse model and revealed that absence of functional DICER in differentiating male germ cells induces disorganization of the cell-cell junctions in the seminiferous epithelium. We detected discontinuous and irregular apical ectoplasmic specializations between elongating spermatids and Sertoli cells. The defective anchoring of spermatids to Sertoli cells caused a premature release of spermatids into the lumen. Our findings may help also explain the abnormal elongation process of remaining spermatids because these junctions and the correct positioning of germ cells in the epithelium are critically important for the progression of spermiogenesis. Interestingly, cell adhesion-related genes were generally upregulated in Dicer1 knockout germ cells. Claudin 5 ( Cldn5 ) was among the most upregulated genes and we show that the polarized localization of CLAUDIN5 in the apical ectoplasmic specializations was lost in Dicer1 knockout spermatids. Our results suggest that DICER-dependent pathways control the formation and organization of cell-cell junctions in the seminiferous epithelium via the regulation of cell adhesion-related genes</description>
<date>2015-01</date>
</dc>
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