Moz and retinoic acid coordinately regulate H3K9 acetylation, Hox gene expression, and segment identity

Developmental Cell
Anne K VossTim Thomas

Abstract

We report that embryos deficient in the histone acetyltransferase Moz (Myst3/Kat6a) show histone H3 lysine 9 (H3K9) hypoacetylation, corresponding H3K9 hypermethylation, and reduced transcription at Hox gene loci. Consistent with an observed caudal shift in Hox gene expression, segment identity is shifted anteriorly, such that Moz-deficient mice show a profound homeotic transformation of the axial skeleton and the nervous system. Intriguingly, histone acetylation defects are relatively specific to H3K9 at Hox loci, as neither Hox H3K14 acetylation nor bulk H3K9 acetylation levels throughout the genome are strongly affected; H4K16 acetylation actually increases in the absence of Moz. H3K9 hypoacetylation, Hox gene repression, and the homeotic transformation caused by lack of Moz are all reversed by treatment with retinoic acid (RA). In conclusion, our data show that Moz regulates H3K9 acetylation at Hox gene loci and that RA can act independently of Moz to establish specific Hox gene expression boundaries.

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Citations

Dec 15, 2010·Molecular and Cellular Biology·Andrew J KuehTim Thomas
Dec 7, 2011·Molecular and Cellular Biology·Nikita AvvakumovJacques Côté
Sep 26, 2013·Genes & Development·Marie-Eve LalondeJacques Côté
Dec 7, 2010·Cellular and Molecular Life Sciences : CMLS·Vasileia Sapountzi, Jacques Côté
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Jul 1, 2014·Proceedings of the National Academy of Sciences of the United States of America·Kim L Good-JacobsonDavid Tarlinton
Apr 30, 2015·Proceedings of the National Academy of Sciences of the United States of America·Bilal N SheikhAnne K Voss
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Sep 3, 2013·Biochimica Et Biophysica Acta·Anne LargeotLaurent Delva
Apr 29, 2015·Developmental Biology·Hannah K VanyaiAnne K Voss
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