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Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development
Testis development and sustained germ cell production in adults rely on the establishment and maintenance of spermatogonia stem cells and their proper differentiation into spermatocytes. Chromatin remodeling complexes regulate critical processes during gamete development by restricting or promoting...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9107693/ https://www.ncbi.nlm.nih.gov/pubmed/35568926 http://dx.doi.org/10.1186/s13072-022-00448-5 |
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author | de Castro, Rodrigo O. Carbajal, Agustin Previato de Almeida, Luciana Goitea, Victor Griffin, Courtney T. Pezza, Roberto J. |
author_facet | de Castro, Rodrigo O. Carbajal, Agustin Previato de Almeida, Luciana Goitea, Victor Griffin, Courtney T. Pezza, Roberto J. |
author_sort | de Castro, Rodrigo O. |
collection | PubMed |
description | Testis development and sustained germ cell production in adults rely on the establishment and maintenance of spermatogonia stem cells and their proper differentiation into spermatocytes. Chromatin remodeling complexes regulate critical processes during gamete development by restricting or promoting accessibility of DNA repair and gene expression machineries to the chromatin. Here, we investigated the role of Chd4 and Chd3 catalytic subunits of the NURD complex during spermatogenesis. Germ cell-specific deletion of chd4 early in gametogenesis, but not chd3, resulted in arrested early gamete development due to failed cell survival of neonate undifferentiated spermatogonia stem cell population. Candidate assessment revealed that Chd4 controls expression of dmrt1 and its downstream target plzf, both described as prominent regulators of spermatogonia stem cell maintenance. Our results show the requirement of Chd4 in mammalian gametogenesis pointing to functions in gene expression early in the process. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13072-022-00448-5. |
format | Online Article Text |
id | pubmed-9107693 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-91076932022-05-16 Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development de Castro, Rodrigo O. Carbajal, Agustin Previato de Almeida, Luciana Goitea, Victor Griffin, Courtney T. Pezza, Roberto J. Epigenetics Chromatin Research Testis development and sustained germ cell production in adults rely on the establishment and maintenance of spermatogonia stem cells and their proper differentiation into spermatocytes. Chromatin remodeling complexes regulate critical processes during gamete development by restricting or promoting accessibility of DNA repair and gene expression machineries to the chromatin. Here, we investigated the role of Chd4 and Chd3 catalytic subunits of the NURD complex during spermatogenesis. Germ cell-specific deletion of chd4 early in gametogenesis, but not chd3, resulted in arrested early gamete development due to failed cell survival of neonate undifferentiated spermatogonia stem cell population. Candidate assessment revealed that Chd4 controls expression of dmrt1 and its downstream target plzf, both described as prominent regulators of spermatogonia stem cell maintenance. Our results show the requirement of Chd4 in mammalian gametogenesis pointing to functions in gene expression early in the process. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13072-022-00448-5. BioMed Central 2022-05-14 /pmc/articles/PMC9107693/ /pubmed/35568926 http://dx.doi.org/10.1186/s13072-022-00448-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research de Castro, Rodrigo O. Carbajal, Agustin Previato de Almeida, Luciana Goitea, Victor Griffin, Courtney T. Pezza, Roberto J. Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development |
title | Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development |
title_full | Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development |
title_fullStr | Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development |
title_full_unstemmed | Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development |
title_short | Mouse Chd4-NURD is required for neonatal spermatogonia survival and normal gonad development |
title_sort | mouse chd4-nurd is required for neonatal spermatogonia survival and normal gonad development |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9107693/ https://www.ncbi.nlm.nih.gov/pubmed/35568926 http://dx.doi.org/10.1186/s13072-022-00448-5 |
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