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X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility
Mammalian sex chromosomes are enriched for large, nearly-identical, palindromic sequences harboring genes expressed predominately in testicular germ cells. Discerning if individual palindrome-associated gene families are essential for male reproduction is difficult due to challenges in disrupting al...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122934/ https://www.ncbi.nlm.nih.gov/pubmed/35595785 http://dx.doi.org/10.1038/s41598-022-12433-9 |
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author | Stark-Dykema, Evan R. Dulka, Eden A. Gerlinger, Emma R. Mueller, Jacob L. |
author_facet | Stark-Dykema, Evan R. Dulka, Eden A. Gerlinger, Emma R. Mueller, Jacob L. |
author_sort | Stark-Dykema, Evan R. |
collection | PubMed |
description | Mammalian sex chromosomes are enriched for large, nearly-identical, palindromic sequences harboring genes expressed predominately in testicular germ cells. Discerning if individual palindrome-associated gene families are essential for male reproduction is difficult due to challenges in disrupting all copies of a gene family. Here we generate precise, independent, deletions to assess the reproductive roles of two X-linked palindromic gene families with spermatid-predominant expression, 4930567H17Rik and Mageb5. Sequence analyses reveals mouse 4930567H17Rik and Mageb5 are orthologs of human HSFX3 and MAGEB5, respectively, where 4930567H17Rik/HSFX3 is harbored in a palindrome in humans and mice, while Mageb5 is not. Additional sequence analyses show 4930567H17Rik and HSFX3 are rapidly diverging in rodents and primates, respectively. Mice lacking either 4930567H17Rik or Mageb5 gene families do not have detectable defects in male fertility, fecundity, spermatogenesis, or in gene regulation, but do show differences in sperm head morphology, suggesting a potential role in sperm function. We conclude that while all palindrome-associated gene families are not essential for male fertility, large palindromes influence the evolution of their associated gene families. |
format | Online Article Text |
id | pubmed-9122934 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-91229342022-05-22 X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility Stark-Dykema, Evan R. Dulka, Eden A. Gerlinger, Emma R. Mueller, Jacob L. Sci Rep Article Mammalian sex chromosomes are enriched for large, nearly-identical, palindromic sequences harboring genes expressed predominately in testicular germ cells. Discerning if individual palindrome-associated gene families are essential for male reproduction is difficult due to challenges in disrupting all copies of a gene family. Here we generate precise, independent, deletions to assess the reproductive roles of two X-linked palindromic gene families with spermatid-predominant expression, 4930567H17Rik and Mageb5. Sequence analyses reveals mouse 4930567H17Rik and Mageb5 are orthologs of human HSFX3 and MAGEB5, respectively, where 4930567H17Rik/HSFX3 is harbored in a palindrome in humans and mice, while Mageb5 is not. Additional sequence analyses show 4930567H17Rik and HSFX3 are rapidly diverging in rodents and primates, respectively. Mice lacking either 4930567H17Rik or Mageb5 gene families do not have detectable defects in male fertility, fecundity, spermatogenesis, or in gene regulation, but do show differences in sperm head morphology, suggesting a potential role in sperm function. We conclude that while all palindrome-associated gene families are not essential for male fertility, large palindromes influence the evolution of their associated gene families. Nature Publishing Group UK 2022-05-20 /pmc/articles/PMC9122934/ /pubmed/35595785 http://dx.doi.org/10.1038/s41598-022-12433-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This 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/) . |
spellingShingle | Article Stark-Dykema, Evan R. Dulka, Eden A. Gerlinger, Emma R. Mueller, Jacob L. X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility |
title | X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility |
title_full | X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility |
title_fullStr | X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility |
title_full_unstemmed | X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility |
title_short | X-linked palindromic gene families 4930567H17Rik and Mageb5 are dispensable for male mouse fertility |
title_sort | x-linked palindromic gene families 4930567h17rik and mageb5 are dispensable for male mouse fertility |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122934/ https://www.ncbi.nlm.nih.gov/pubmed/35595785 http://dx.doi.org/10.1038/s41598-022-12433-9 |
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