Deletion of MgcRacGAP in the male germ cells impairs spermatogenesis and causes male sterility in the mouse |
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| Authors: | Patrick Lorè s,Nadè ge Vernet,Tomohiro Kurosaki,Tom Van de Putte,Danny Huylebroeck,Masaki Hikida,Gé rard Gacon,Aminata Touré |
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| Affiliation: | 1. INSERM U1016, Institut Cochin, 75014 Paris, France;2. CNRS UMR8104, 75014 Paris, France;3. Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, 75014 Paris, France;4. Department of functional genomics and cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67404 Illkirch Cedex, France;5. Center for Innovation in Immunoregulative Technology and Therapeutics, AK Project, 606-8501 Kyoto, Japan;6. Laboratory of Molecular Biology (Celgen), Department Development and Regeneration, KU Leuven, 3000 Leuven, Belgium;g Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Japan;h Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Japan |
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| Abstract: | MgcRacGAP (RACGAP1) is a GTPase Activating Protein (GAP), highly produced in the mouse embryonic brain and in the human and mouse post-natal testis. MgcRacGAP negatively controls the activity of Rac and Cdc42, which are key molecular switches acting on the microtubule and actin cytoskeleton and controlling various cell processes such as proliferation, adhesion and motility. Previous studies demonstrated that MgcRacGAP plays a critical role in the cytokinesis of somatic cells; hence homozygous inactivation of the gene in the mouse and mutation in Caenorhabditis elegans led to embryonic lethality due to the inability of MgcRacGAP-null embryos to assemble the central spindle and to complete cytokinesis. |
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| Keywords: | MgcRacGAP Testis Knock out mouse model Spermatogenesis Male infertility |
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