Bonitto Kenya, Sarathy Kirthana, Atai Kaiser, Mitra Mithun, Coller Hilary A
Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, United States.
Molecular Biology Interdepartmental Doctoral Program, University of California, Los Angeles, Los Angeles, CA, United States.
Front Cell Dev Biol. 2021 Oct 29;9:739780. doi: 10.3389/fcell.2021.739780. eCollection 2021.
Many of the cells in our bodies are quiescent, that is, temporarily not dividing. Under certain physiological conditions such as during tissue repair and maintenance, quiescent cells receive the appropriate stimulus and are induced to enter the cell cycle. The ability of cells to successfully transition into and out of a quiescent state is crucial for many biological processes including wound healing, stem cell maintenance, and immunological responses. Across species and tissues, transcriptional, epigenetic, and chromosomal changes associated with the transition between proliferation and quiescence have been analyzed, and some consistent changes associated with quiescence have been identified. Histone modifications have been shown to play a role in chromatin packing and accessibility, nucleosome mobility, gene expression, and chromosome arrangement. In this review, we critically evaluate the role of different histone marks in these processes during quiescence entry and exit. We consider different model systems for quiescence, each of the most frequently monitored candidate histone marks, and the role of their writers, erasers and readers. We highlight data that support these marks contributing to the changes observed with quiescence. We specifically ask whether there is a quiescence histone "code," a mechanism whereby the language encoded by specific combinations of histone marks is read and relayed downstream to modulate cell state and function. We conclude by highlighting emerging technologies that can be applied to gain greater insight into the role of a histone code for quiescence.
我们体内的许多细胞都处于静止状态，也就是说，暂时不进行分裂。在某些生理条件下，如组织修复和维持期间，静止细胞会受到适当的刺激并被诱导进入细胞周期。细胞成功转入和转出静止状态的能力对于许多生物学过程至关重要，包括伤口愈合、干细胞维持和免疫反应。跨物种和组织，与增殖和静止之间转变相关的转录、表观遗传和染色体变化已得到分析，并且已确定了一些与静止相关的一致变化。组蛋白修饰已被证明在染色质包装和可及性、核小体移动性、基因表达和染色体排列中发挥作用。在本综述中，我们批判性地评估了不同组蛋白标记在静止进入和退出过程中这些过程中的作用。我们考虑了静止的不同模型系统、每个最常监测的候选组蛋白标记及其写入器、擦除器和读取器的作用。我们强调支持这些标记导致静止时观察到的变化的数据。我们特别询问是否存在静止组蛋白“密码”，即一种机制，通过该机制，由组蛋白标记的特定组合编码的语言被读取并向下游传递以调节细胞状态和功能。我们通过强调可用于更深入了解静止组蛋白密码作用的新兴技术来得出结论。
