Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
Dev Biol. 2012 Jul 15;367(2):91-9. doi: 10.1016/j.ydbio.2012.04.030. Epub 2012 May 4.
During organogenesis, tissues expand in size and eventually acquire consistent ratios of cells with dazzling diversity in morphology and function. During this process progenitor cells exit the cell cycle and execute differentiation programs through extensive genetic reprogramming that involves the silencing of proliferation genes and the activation of differentiation genes in a step-wise temporal manner. Recent years have witnessed expansion in our understanding of the epigenetic mechanisms that contribute to cellular differentiation and maturation during organ development, as this is a crucial step toward advancing regenerative therapy research for many intractable disorders. Among such epigenetic programs, the developmental roles of the polycomb repressive complex 2 (PRC2), a chromatin remodeling complex that mediates silencing of gene expression, have been under intensive examination. This review summarizes recent findings of how PRC2 functions to regulate the transition from proliferation to differentiation during organogenesis and discusses some aspects of the remaining questions associated with its regulation and mechanisms of action.
在器官发生过程中，组织会扩大体积，最终获得具有惊人多样性的细胞比例，这些细胞在形态和功能上存在差异。在此过程中，祖细胞退出细胞周期，并通过广泛的遗传重编程执行分化程序，该程序涉及增殖基因的沉默和分化基因的激活，这是一个逐步的时间过程。近年来，我们对参与器官发育过程中细胞分化和成熟的表观遗传机制的理解有了扩展，因为这是推进许多难治性疾病再生治疗研究的关键步骤。在这些表观遗传程序中，多梳抑制复合物 2（PRC2）作为一种染色质重塑复合物，介导基因表达的沉默，其在发育中的作用受到了广泛关注。这篇综述总结了最近关于 PRC2 如何在器官发生过程中调节从增殖到分化的转变的发现，并讨论了与它的调节和作用机制相关的一些遗留问题。
