Biparental contributions of the H2A.B histone variant control embryonic development in mice.
Histone variants expand chromatin functions in eukaryote genomes. H2A.B genes are testis-expressed short histone H2A variants that arose in placental mammals. Their biological functions remain largely unknown. To investigate their function, we generated a knockout (KO) model that disrupts all 3 H2A....
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2020-12-01
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Online Access: | https://doi.org/10.1371/journal.pbio.3001001 |
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doaj-839f80c3c6cb4d0b958744b6ee3c8b6d2021-07-02T18:07:21ZengPublic Library of Science (PLoS)PLoS Biology1544-91731545-78852020-12-011812e300100110.1371/journal.pbio.3001001Biparental contributions of the H2A.B histone variant control embryonic development in mice.Antoine MolaroAnna J WoodDerek JanssensSelina M KindelayMichael T EickbushSteven WuPriti SinghCharles H MullerSteven HenikoffHarmit S MalikHistone variants expand chromatin functions in eukaryote genomes. H2A.B genes are testis-expressed short histone H2A variants that arose in placental mammals. Their biological functions remain largely unknown. To investigate their function, we generated a knockout (KO) model that disrupts all 3 H2A.B genes in mice. We show that H2A.B KO males have globally altered chromatin structure in postmeiotic germ cells. Yet, they do not show impaired spermatogenesis or testis function. Instead, we find that H2A.B plays a crucial role postfertilization. Crosses between H2A.B KO males and females yield embryos with lower viability and reduced size. Using a series of genetic crosses that separate parental and zygotic contributions, we show that the H2A.B status of both the father and mother, but not of the zygote, affects embryonic viability and growth during gestation. We conclude that H2A.B is a novel parental-effect gene, establishing a role for short H2A histone variants in mammalian development. We posit that parental antagonism over embryonic growth drove the origin and ongoing diversification of short histone H2A variants in placental mammals.https://doi.org/10.1371/journal.pbio.3001001 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Antoine Molaro Anna J Wood Derek Janssens Selina M Kindelay Michael T Eickbush Steven Wu Priti Singh Charles H Muller Steven Henikoff Harmit S Malik |
spellingShingle |
Antoine Molaro Anna J Wood Derek Janssens Selina M Kindelay Michael T Eickbush Steven Wu Priti Singh Charles H Muller Steven Henikoff Harmit S Malik Biparental contributions of the H2A.B histone variant control embryonic development in mice. PLoS Biology |
author_facet |
Antoine Molaro Anna J Wood Derek Janssens Selina M Kindelay Michael T Eickbush Steven Wu Priti Singh Charles H Muller Steven Henikoff Harmit S Malik |
author_sort |
Antoine Molaro |
title |
Biparental contributions of the H2A.B histone variant control embryonic development in mice. |
title_short |
Biparental contributions of the H2A.B histone variant control embryonic development in mice. |
title_full |
Biparental contributions of the H2A.B histone variant control embryonic development in mice. |
title_fullStr |
Biparental contributions of the H2A.B histone variant control embryonic development in mice. |
title_full_unstemmed |
Biparental contributions of the H2A.B histone variant control embryonic development in mice. |
title_sort |
biparental contributions of the h2a.b histone variant control embryonic development in mice. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS Biology |
issn |
1544-9173 1545-7885 |
publishDate |
2020-12-01 |
description |
Histone variants expand chromatin functions in eukaryote genomes. H2A.B genes are testis-expressed short histone H2A variants that arose in placental mammals. Their biological functions remain largely unknown. To investigate their function, we generated a knockout (KO) model that disrupts all 3 H2A.B genes in mice. We show that H2A.B KO males have globally altered chromatin structure in postmeiotic germ cells. Yet, they do not show impaired spermatogenesis or testis function. Instead, we find that H2A.B plays a crucial role postfertilization. Crosses between H2A.B KO males and females yield embryos with lower viability and reduced size. Using a series of genetic crosses that separate parental and zygotic contributions, we show that the H2A.B status of both the father and mother, but not of the zygote, affects embryonic viability and growth during gestation. We conclude that H2A.B is a novel parental-effect gene, establishing a role for short H2A histone variants in mammalian development. We posit that parental antagonism over embryonic growth drove the origin and ongoing diversification of short histone H2A variants in placental mammals. |
url |
https://doi.org/10.1371/journal.pbio.3001001 |
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