Author response: An H3K9 methylation-dependent protein interaction regulates the non-enzymatic functions of a putative histone demethylase

Raiymbek, Gulzhan; An, Soon Il; Khurana, Nidhi; Gopinath, Saarang; Larkin, Ajay; Biswas, Saikat; Trievel, Raymond C.; Cho, Uhn‐Soo; Ragunathan, Kaushik

doi:10.7554/elife.53155.sa2

Cited by 2 publications

(3 citation statements)

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“…S4E). We conclude that the specific suppression of heterochromatin spreading by epe1D in the FACT mutants is related to the role of Epe1 in nucleosome stability regulation, in agreement with a recent study (Raiymbek et al, 2020). Altogether, our data indicate that FACT regulates heterochromatin spreading by promoting the transition of H3K9me2 to H3K9me3 through histone turnover suppression.…”

Section: Fact Promotes the Transition Of H3k9me2 To H3k9me3 Through Histone Turnover Suppressionsupporting

confidence: 93%

The histone chaperone FACT facilitates heterochromatin spreading through regulation of histone turnover and H3K9 methylation states

Murawska

Greenstein

Schauer

et al. 2021

Preprint

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Heterochromatin formation requires three distinct steps: nucleation, self-propagation (spreading) along the chromosome, and faithful maintenance after each replication cycle. Impeding any of those steps induces heterochromatin defects and improper gene expression. The essential histone chaperone FACT has been implicated in heterochromatin silencing, however, the mechanisms by which FACT engages in this process remain opaque. Here, we pin-pointed its function to the heterochromatin spreading process. FACT impairment reduces nucleation-distal H3K9me3 and HP1/Swi6 accumulation at subtelomeres and de-represses genes in the vicinity of heterochromatin boundaries. FACT promotes spreading by repressing heterochromatic histone turnover, which is crucial for the H3K9me2 to me3 transition that enables spreading. FACT mutant spreading defects are suppressed by removal of the H3K9 methylation antagonist Epe1 via nucleosome stabilization. Together, our study identifies FACT as a histone chaperone that specifically promotes heterochromatin spreading and lends support to the model that regulated histone turnover controls the propagation of epigenetic marks.

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Section: Fact Promotes the Transition Of H3k9me2 To H3k9me3 Through Histone Turnover Suppressionsupporting

confidence: 93%

The histone chaperone FACT facilitates heterochromatin spreading through regulation of histone turnover and H3K9 methylation states

Murawska

Greenstein

Schauer

et al. 2021

Preprint

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“…Histone modifications alter the structure of nucleosomes, regulate gene transcription, and mediate growth and disease pathogenesis (29,30). The important and unique roles of these histone modifications have been reported by a number of studies (31,32).…”

Section: Histone Methylation Modificationmentioning

confidence: 99%

“…Histone H3 and H4 can undergo methylation modification, and the methylation and demethylation of different sites are mediated by specific enzymes (Figure 1). In humans, the following two protein domains carry out lysine methylation: SET domain [named after three Drosophila melanogaster proteins originally recognized as containing this domain, namely, Su(var)3-9, Enhancer of zeste, and Trithorax] and the seven beta-strand (7βS) domain [non-SET-domain enzymes; (30,31)]. These two families account for more than 200 enzymes with different amino acid residue specificity (48).…”

Section: Histone Methylation Modificationmentioning

confidence: 99%

Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases

Yang

Luan

Yuan

et al. 2021

Front. Cardiovasc. Med.

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The epidemic of cardiovascular diseases (CVDs) is predicted to spread rapidly in advanced countries accompanied by the high prevalence of risk factors. In terms of pathogenesis, the pathophysiology of CVDs is featured by multiple disorders, including vascular inflammation accompanied by simultaneously perturbed pathways, such as cell death and acute/chronic inflammatory reactions. Epigenetic alteration is involved in the regulation of genome stabilization and cellular homeostasis. The association between CVD progression and histone modifications is widely known. Among the histone modifications, histone methylation is a reversible process involved in the development and homeostasis of the cardiovascular system. Abnormal methylation can promote CVD progression. This review discusses histone methylation and the enzymes involved in the cardiovascular system and determine the effects of histone methyltransferases and demethylases on the pathogenesis of CVDs. We will further demonstrate key proteins mediated by histone methylation in blood vessels and review histone methylation-mediated cardiomyocytes and cellular functions and pathways in CVDs. Finally, we will summarize the role of inhibitors of histone methylation and demethylation in CVDs and analyze their therapeutic potential, based on previous studies.

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Author response: An H3K9 methylation-dependent protein interaction regulates the non-enzymatic functions of a putative histone demethylase

Cited by 2 publications

References 0 publications

The histone chaperone FACT facilitates heterochromatin spreading through regulation of histone turnover and H3K9 methylation states

The histone chaperone FACT facilitates heterochromatin spreading through regulation of histone turnover and H3K9 methylation states

Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases

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