Histone lysine methyltransferase Pr‐set7/SETD8 promotes neural stem cell reactivation

Huang, Jiawen; Gujar, Mahekta R; Deng, Qiannan; Chia, Sook Yoong; Li, Song; Tan, Patrick; Sung, Wing‐Kin; Wang, Hongyan

doi:10.15252/embr.202050994

Cited by 19 publications

(26 citation statements)

References 87 publications

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“…Thus, by increasing expression of Cdk1 and Ebd1 in NSCs, Pr-set7 modulates the cell cycle and Wnt signaling, and thereby promotes NSC reactivation from quiescence (Huang et al, 2021). In these studies, The presence or absence of H4K20me1 in Ebd1 and Cdk1 promoters was not determined in this study (Huang et al, 2021).…”

Section: H4 Methylation With Quiescencementioning

confidence: 81%

“…H4K20me1 can act both as a repressive and an activating mark (Huang et al, 2021). On one hand, H4K20me1 causes chromatin condensation (Lu et al, 2008;Oda et al, 2009), and in mammalian cells, can recruit L3MBTL1, a H4K20me1 reader that can induce nucleosome compaction .…”

Section: H4 Methylation With Quiescencementioning

confidence: 99%

“…The H4K20 monomethyltransferase Pr-set-7 was discovered to regulate NSC quiescence in Drosophila (Huang et al, 2021). Targeted DNA adenine methyltransferase identification (TaDa) was used to determine genomic loci where Pr-set7 binds.…”

Section: H4 Methylation With Quiescencementioning

confidence: 99%

“…Targeted DNA adenine methyltransferase identification (TaDa) was used to determine genomic loci where Pr-set7 binds. This analysis revealed Pr-set-7 binds to the promoter and transcriptional start sites of Wnt pathway coactivator earthbound1 (Ebd1) and cyclin-dependent kinase 1 (Cdk1) (Huang et al, 2021). The mRNA levels of Ebd1 and Cdk1 were depleted in pr-set7 mutant brains (Huang et al, 2021).…”

Section: H4 Methylation With Quiescencementioning

confidence: 99%

“…This analysis revealed Pr-set-7 binds to the promoter and transcriptional start sites of Wnt pathway coactivator earthbound1 (Ebd1) and cyclin-dependent kinase 1 (Cdk1) (Huang et al, 2021). The mRNA levels of Ebd1 and Cdk1 were depleted in pr-set7 mutant brains (Huang et al, 2021). Thus, by increasing expression of Cdk1 and Ebd1 in NSCs, Pr-set7 modulates the cell cycle and Wnt signaling, and thereby promotes NSC reactivation from quiescence (Huang et al, 2021).…”

Section: H4 Methylation With Quiescencementioning

confidence: 99%

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Is There a Histone Code for Cellular Quiescence?

Bonitto

Sarathy

Atai

et al. 2021

Front. Cell Dev. Biol.

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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.

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Section: H4 Methylation With Quiescencementioning

confidence: 81%

Section: H4 Methylation With Quiescencementioning

confidence: 99%

Section: H4 Methylation With Quiescencementioning

confidence: 99%

Section: H4 Methylation With Quiescencementioning

confidence: 99%

Section: H4 Methylation With Quiescencementioning

confidence: 99%

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Is There a Histone Code for Cellular Quiescence?

Bonitto

Sarathy

Atai

et al. 2021

Front. Cell Dev. Biol.

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Genistein-induced Anticancer Effects on Acute Leukemia Cells Involve the Regulation of Wnt Signaling Pathway Through H4K20me1 Rather Than DNA Demethylation

Zhou

Shen

et al. 2021

CURR MED SCI

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Objective To investigate the effects and mechanisms of genistein on the gene expression in the Wnt pathway in acute leukemia (AL) cells. Methods The expression of Wnt pathway genes and cell cycle-related genes were analyzed in two AL cell lines. Pyrophosphate sequencing was performed to determine the methylation degree. Then, the enrichment of H4K20me1 and H3K9ac was determined using ChIP-qPCR. Flow cytometry was used to analyze the cell cycle. Results The IC50 of genistein in the two AL cell lines was lower than that for the bone marrow mesenchymal stem cell line. Genistein upregulated H4K20me1, KMT5A and Wnt suppressor genes, including Wnt5a, and downregulated the downstream target genes of Wnt, such as c-myc and β-catenin. The methylation degree and H3K9ac enrichment in the Wnt5a promoter region remained unchanged. However, the enrichment of H4K20me1 in the Wnt5a promoter and coding regions increased. In addition, genistein upregulated Phospho-cdc2, Myt1, Cyclin A, Cyclin E2, p21 and Phospho-histone H3, but downregulated Phospho-wee1. Cell cycle arrest was induced in the G2/M phase. Conclusion Genistein inhibits the activation of the Wnt pathway by promoting the expression of Wnt5a through the activation of KMT5A and enrichment of H4K20me1 in the Wnt5a gene promoter and coding regions, rather than demethylation. Genistein also blocks the cell cycle in the G2/M phase. Therefore, genistein is a potential anti-leukemia drug.

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