Asymmetric Histone Inheritance Regulates Stem Cell Fate in Drosophila Midgut

Chen, Xin; Zion, Emily

doi:10.2139/ssrn.3671969

Cited by 3 publications

(2 citation statements)

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“…Whether the CENP-A asymmetry dictates spermatogonial cell fate or if CENP-A levels serve as biomarker for the fate of the spermatogonial cells are intriguing questions and will be an active area of further investigation. Asymmetric segregation of H3 and H4 (old vs. new) as well as and CENP-A is a hallmark of asymmetric cell division identified in Drosophila male germline stem cells (Ranjan et al, 2019; Tran et al, 2012) and in Drosophila intestinal stem cells (Chen and Zion, 2020; García del Arco et al, 2018). CENP-A was also found to be inherited asymmetrically in female germline stem cells (Dattoli et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Equalizing epigenetically imprinted centromeres in early mammalian embryos

Manske

Jorgensen

et al. 2022

Preprint

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The CENP-A histone variant epigenetically defines centromeres, where its levels and locations are precisely maintained through mitotic cell divisions. However, differences in centromere CENP-A propagation in soma versus female/male germline remains poorly understood. Here, we generated CenpamScarlet mice and followed CENP-A dynamics in gametes, zygotes, and embryos. We found that, unlike somatic cells, progenitor female and male germ cells carry high centromeric CENP-A levels that decrease upon terminal differentiation. The reduction in CENP-A is differentially regulated between sexes, resulting in a ten-fold higher level in oocytes compared to sperm. In the zygote, the parent-of-origin CENP-A asymmetry is equalized prior to initial S-phase by redistribution of nuclear CENP-A from maternal to paternal chromosomes. Redistribution of CENP-A requires both CDK1/2 and PLK1 centromeric machinery. These experiments provide direct evidence for resetting of epigenetically imprinted centromeres in early pronuclear stage embryos and imply a mechanism to sense the non-equivalency of parental chromosomes.

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Section: Discussionmentioning

confidence: 99%

Equalizing epigenetically imprinted centromeres in early mammalian embryos

Manske

Jorgensen

et al. 2022

Preprint

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“…After the initial discovery in the Drosophila male GSC system, it became of great interest to examine the generality of this phenomenon and how it may regulate cell fate decisions in different systems and developmental contexts. Recently, it has been reported that global asymmetric histone inheritance also occurs in asymmetrically dividing Drosophila ISCs [ 120 ]. Similar to the male GSCs, old H3 and H4 are predominantly inherited by the self-renewed ISCs, while new histones are inherited by the differentiating daughter cells.…”

Section: Histone Inheritance Modes In Other Systemsmentioning

confidence: 99%

Mitotic drive in asymmetric epigenetic inheritance

Ranjan

Chen

2022

Biochemical Society Transactions

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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.

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