Nucleosome proteostasis and histone turnover.
Nucleosome proteostasis and histone turnover.
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DOI：
10.3389/fmolb.2022.990006
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发表时间：
2022
影响因子：
5
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中科院分区：
文献类型：
--
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蛋白质折叠稳态的维持对细胞存活以及细胞类型特异性生物过程的执行至关重要，如肌肉细胞收缩性、神经元突触和记忆的形成，以及细胞从有丝分裂细胞类型向有丝分裂后细胞类型的转变。细胞类型规范主要由染色质组织驱动，染色质组织根据细胞的需要和功能决定哪些基因被关闭或打开。染色质组织的丧失可能对细胞存活或细胞类型特异性功能造成灾难性的后果。染色质的组织高度依赖于核小体的组织、时空核小体的组装和拆卸以及组蛋白的周转。在这篇综述中，我们的目标是强调为什么核小体蛋白平衡对染色质组织至关重要，这一过程是如何由组蛋白伴侣和atp依赖性染色质重塑蛋白介导的，并概述疾病期间核小体蛋白平衡被破坏的潜在和已建立的机制。最后，我们强调了组蛋白转换和核小体蛋白静止的这些机制如何与未折叠的蛋白反应程序共同驱动细胞生长和发育中的组蛋白转换。
Maintenance of protein folding homeostasis, or proteostasis is critical for cell survival as well as for execution of cell type specific biological processes such as muscle cell contractility, neuronal synapse and memory formation, and cell transition from a mitotic to post-mitotic cell type. Cell type specification is driven largely by chromatin organization, which dictates which genes are turned off or on, depending on cell needs and function. Loss of chromatin organization can have catastrophic consequences either on cell survival or cell type specific function. Chromatin organization is highly dependent on organization of nucleosomes, spatiotemporal nucleosome assembly and disassembly, and histone turnover. In this review our goal is to highlight why nucleosome proteostasis is critical for chromatin organization, how this process is mediated by histone chaperones and ATP-dependent chromatin remodelers and outline potential and established mechanisms of disrupted nucleosome proteostasis during disease. Finally, we highlight how these mechanisms of histone turnover and nucleosome proteostasis may conspire with unfolded protein response programs to drive histone turnover in cell growth and development.