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首页> 外文期刊>Developmental cell >The polycomb complex protein mes-2/E(z) promotes the transition from developmental plasticity to differentiation in C. elegans embryos.
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The polycomb complex protein mes-2/E(z) promotes the transition from developmental plasticity to differentiation in C. elegans embryos.

机译：polycomb复合蛋白mes-2 / E（z）促进秀丽隐杆线虫胚胎从发育可塑性过渡到分化。

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We have used expression profiling and in vivo imaging to characterize Caenorhabditis elegans embryos as they transit from a developmentally plastic state to the onset of differentiation. Normally, this transition is accompanied by activation of developmental regulators and differentiation genes, downregulation of early-expressed genes, and large-scale reorganization of chromatin. We find that loss of plasticity and differentiation onset depends on the Polycomb complex protein mes-2/E(Z). mes-2 mutants display prolonged developmental plasticity in response to heterologous developmental regulators. Early-expressed genes remain active, differentiation genes fail to reach wild-type levels, and chromatin retains a decompacted morphology in mes-2 mutants. By contrast, loss of the developmental regulators pha-4/FoxA or end-1/GATA does not prolong plasticity. This study establishes a model by which to analyze developmental plasticity within an intact embryo. mes-2 orchestrates large-scale changes in chromatin organization and gene expression to promote the timely loss of developmental plasticity. Our findings indicate that loss of plasticity can be uncoupled from cell fate specification.
机译：我们已经使用表达谱和体内成像来表征秀丽隐杆线虫胚胎，因为它们从发育可塑性状态过渡到分化开始。通常，这种转变伴随着发育调节剂和分化基因的激活，早期表达基因的下调以及染色质的大规模重组。我们发现可塑性和分化开始的损失取决于Polycomb复杂蛋白mes-2 / E（Z）。 mes-2突变体对异源发育调节剂的响应显示出延长的发育可塑性。早期表达的基因保持活跃，分化基因无法达到野生型水平，染色质在mes-2突变体中保留了紧凑的形态。相反，丧失发育调节因子pha-4 / FoxA或end-1 / GATA不会延长可塑性。这项研究建立了一个模型，通过该模型可以分析完整胚胎内的发育可塑性。 mes-2协调染色质组织和基因表达的大规模变化，以促进发育可塑性的及时丧失。我们的发现表明，可塑性的丧失可以与细胞命运的规范脱钩。

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