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Development February 1, 2013; 140 (4): 853-60.

Optimal histone H3 to linker histone H1 chromatin ratio is vital for mesodermal competence in Xenopus.

Lim CY , Reversade B , Knowles BB , Solter D .

Cellular differentiation during embryogenesis involves complex gene regulation to enable the activation and repression of genes. Here, we show that mesodermal competence is inhibited in Xenopus embryos depleted of histones H3 and H3.3, which fail to respond to Nodal/Activin signaling and exhibit concomitant loss of mesodermal gene expression. We find that transcriptional activation in gastrula embryos does not correlate with promoter deposition of H3.3. Instead, gastrulation defects in H3.3/H3-deficient embryos are partially rescued with concurrent depletion of the linker histone H1A. In addition, we show that linker histone H1-induced premature loss of mesodermal competence in animal cap explants can be abrogated with the overexpression of nucleosomal H3.3/H3. Our findings establish a chromatin-mediated regulatory mechanism in which a threshold level of H3 is required to prevent H1-induced gene repression, and thus facilitate mesodermal differentiation in response to inductive signaling.

PubMed ID: 23318639
Article link: Development

Genes referenced: aldh1a2 cebpa cer1 chrd.1 dlc eomes foxi1 gsc h1-3 h2az1 h3-3a h3-3b hhex inhba krt12.4 lhx1 mespa mix1 myf5 nodal nodal1 nrl odc1 sia1 smad1 smad2 sox17a tbx6 tbxt wnt8a
Morpholinos: h3f3a MO1 h3f3a MO2

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