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有丝分裂驱动的非对称表观遗传遗传。

Mitotic drive in asymmetric epigenetic inheritance.

机构信息

Howard Hughes Medical Institute, Department of Biology, The Johns Hopkins University, 3400 North Charles Street, Baltimore, MD 21218-2685, U.S.A.

出版信息

Biochem Soc Trans. 2022 Apr 29;50(2):675-688. doi: 10.1042/BST20200267.

DOI:10.1042/BST20200267
PMID:35437581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9162470/
Abstract

Asymmetric cell division (ACD) produces two daughter cells with distinct cell fates. This division mode is widely used during development and by adult stem cells during tissue homeostasis and regeneration, which can be regulated by both extrinsic cues such as signaling molecules and intrinsic factors such as epigenetic information. While the DNA replication process ensures that the sequences of sister chromatids are identical, how epigenetic information is re-distributed during ACD has remained largely unclear in multicellular organisms. Studies of Drosophila male germline stem cells (GSCs) have revealed that sister chromatids incorporate pre-existing and newly synthesized histones differentially and segregate asymmetrically during ACD. To understand the underlying molecular mechanisms of this phenomenon, two key questions must be answered: first, how and when asymmetric histone information is established; and second, how epigenetically distinct sister chromatids are distinguished and segregated. Here, we discuss recent advances which help our understanding of this interesting and important cell division mode.

摘要

不对称细胞分裂(ACD)产生具有不同细胞命运的两个子细胞。这种分裂模式在发育过程中广泛使用,并且在组织内稳态和再生过程中由成年干细胞使用,其可以受到信号分子等外在线索和表观遗传信息等内在因素的调节。虽然 DNA 复制过程确保姐妹染色单体的序列完全相同,但在多细胞生物中,ACD 过程中表观遗传信息如何重新分配在很大程度上仍不清楚。对果蝇雄性生殖干细胞(GSCs)的研究表明,姐妹染色单体在 ACD 过程中以不同的方式掺入预先存在的和新合成的组蛋白,并进行不对称分配。为了了解这一现象的潜在分子机制,必须回答两个关键问题:首先,不对称组蛋白信息是如何以及何时建立的;其次,如何区分和分离具有不同表观遗传特征的姐妹染色单体。在这里,我们讨论了有助于我们理解这种有趣和重要的细胞分裂模式的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/30e2671dc92f/BST-50-675-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/095e1c989e02/BST-50-675-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/33006de55523/BST-50-675-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/30e2671dc92f/BST-50-675-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/095e1c989e02/BST-50-675-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/33006de55523/BST-50-675-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f19/9162470/30e2671dc92f/BST-50-675-g0003.jpg

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PLoS Genet. 2021 May 20;17(5):e1009247. doi: 10.1371/journal.pgen.1009247. eCollection 2021 May.
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