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Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice
Hybrid sterility is one of the reproductive isolation mechanisms leading to speciation. Prdm9, the only known vertebrate hybrid-sterility gene, causes failure of meiotic chromosome synapsis and infertility in male hybrids that are the offspring of two mouse subspecies. Within species, Prdm9 determin...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5902161/ https://www.ncbi.nlm.nih.gov/pubmed/29537370 http://dx.doi.org/10.7554/eLife.34282 |
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author | Gregorova, Sona Gergelits, Vaclav Chvatalova, Irena Bhattacharyya, Tanmoy Valiskova, Barbora Fotopulosova, Vladana Jansa, Petr Wiatrowska, Diana Forejt, Jiri |
author_facet | Gregorova, Sona Gergelits, Vaclav Chvatalova, Irena Bhattacharyya, Tanmoy Valiskova, Barbora Fotopulosova, Vladana Jansa, Petr Wiatrowska, Diana Forejt, Jiri |
author_sort | Gregorova, Sona |
collection | PubMed |
description | Hybrid sterility is one of the reproductive isolation mechanisms leading to speciation. Prdm9, the only known vertebrate hybrid-sterility gene, causes failure of meiotic chromosome synapsis and infertility in male hybrids that are the offspring of two mouse subspecies. Within species, Prdm9 determines the sites of programmed DNA double-strand breaks (DSBs) and meiotic recombination hotspots. To investigate the relation between Prdm9-controlled meiotic arrest and asynapsis, we inserted random stretches of consubspecific homology on several autosomal pairs in sterile hybrids, and analyzed their ability to form synaptonemal complexes and to rescue male fertility. Twenty-seven or more megabases of consubspecific (belonging to the same subspecies) homology fully restored synapsis in a given autosomal pair, and we predicted that two or more DSBs within symmetric hotspots per chromosome are necessary for successful meiosis. We hypothesize that impaired recombination between evolutionarily diverged chromosomes could function as one of the mechanisms of hybrid sterility occurring in various sexually reproducing species. |
format | Online Article Text |
id | pubmed-5902161 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-59021612018-04-18 Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice Gregorova, Sona Gergelits, Vaclav Chvatalova, Irena Bhattacharyya, Tanmoy Valiskova, Barbora Fotopulosova, Vladana Jansa, Petr Wiatrowska, Diana Forejt, Jiri eLife Chromosomes and Gene Expression Hybrid sterility is one of the reproductive isolation mechanisms leading to speciation. Prdm9, the only known vertebrate hybrid-sterility gene, causes failure of meiotic chromosome synapsis and infertility in male hybrids that are the offspring of two mouse subspecies. Within species, Prdm9 determines the sites of programmed DNA double-strand breaks (DSBs) and meiotic recombination hotspots. To investigate the relation between Prdm9-controlled meiotic arrest and asynapsis, we inserted random stretches of consubspecific homology on several autosomal pairs in sterile hybrids, and analyzed their ability to form synaptonemal complexes and to rescue male fertility. Twenty-seven or more megabases of consubspecific (belonging to the same subspecies) homology fully restored synapsis in a given autosomal pair, and we predicted that two or more DSBs within symmetric hotspots per chromosome are necessary for successful meiosis. We hypothesize that impaired recombination between evolutionarily diverged chromosomes could function as one of the mechanisms of hybrid sterility occurring in various sexually reproducing species. eLife Sciences Publications, Ltd 2018-03-14 /pmc/articles/PMC5902161/ /pubmed/29537370 http://dx.doi.org/10.7554/eLife.34282 Text en © 2018, Gregorova et al https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Chromosomes and Gene Expression Gregorova, Sona Gergelits, Vaclav Chvatalova, Irena Bhattacharyya, Tanmoy Valiskova, Barbora Fotopulosova, Vladana Jansa, Petr Wiatrowska, Diana Forejt, Jiri Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
title | Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
title_full | Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
title_fullStr | Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
title_full_unstemmed | Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
title_short | Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
title_sort | modulation of prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice |
topic | Chromosomes and Gene Expression |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5902161/ https://www.ncbi.nlm.nih.gov/pubmed/29537370 http://dx.doi.org/10.7554/eLife.34282 |
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