Understanding histone H3 lysine 36 methylation and its deregulation in disease

Li, Jie; Ahn, Jeong Hyun; Wang, Gang Greg

doi:10.1007/s00018-019-03144-y

Cited by 111 publications

(102 citation statements)

References 174 publications

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“…Since we did not knockdown ASH1L at the neuronal progenitor stage our findings do not discount the potential of ASH1L to be involved in cell fate transitions during human corticogenesis. Additionally, we do not discount that additional epigenetic mechanisms could be at play such as the activity of specific histone demethylases that regulate the methylation of lysine 36 (Li et al, 2019a) and could facilitate the activity of the Polycomb complexes.…”

Section: Discussionmentioning

confidence: 92%

“…The current ENCODE data sets lack analysis of H3K36me2 that is primarily deposited by ASH1L. However, H3K36me2 presence will lead to upregulation of H3K36me3 by SET2 (Li et al, 2019a), and H3K4me3 marks are deposited by the ASH1L interactor -MLL complex (Zhu et al, 2016a). Therefore, both H3K36me3 and H3K4me3 marks are highly correlated with the presence of H3K36me2 (Miao and Natarajan, 2005), and were used as correlative evidence for the presence of H3K36me2 marks.…”

Section: Ash1l Specifically Regulates the Expression Of The Neurotropmentioning

confidence: 99%

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ASH1L REGULATES THE STRUCTURAL DEVELOPMENT OF NEURONAL CIRCUITRY BY MODULATING BDNF/TrkB SIGNALING IN HUMAN NEURONS

Cheon

Culver

Bagnell

et al. 2020

Preprint

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Running title: Epigenetic regulation of neurotrophin signaling pathways by ASH1L Cheon, et al 2020 BioRXV eTOC BLURB Cheon et al. report a novel epigenetic mechanism that implicates the counteracting activities of the evolutionarily conserved Trithorax (ASH1L) and Polycomb (PRC2) chromatin regulators, in the modulation of human neuronal connectivity by regulating the developmentally important TrkB-BDNF signaling pathway.

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Section: Discussionmentioning

confidence: 92%

Section: Ash1l Specifically Regulates the Expression Of The Neurotropmentioning

confidence: 99%

ASH1L REGULATES THE STRUCTURAL DEVELOPMENT OF NEURONAL CIRCUITRY BY MODULATING BDNF/TrkB SIGNALING IN HUMAN NEURONS

Cheon

Culver

Bagnell

et al. 2020

Preprint

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“…In addition to the H3G34 mutations, H3K36M mutations, found in over 90% of chondroblastoma cases and in large subgroup of head and neck sarcomas, function as dominant negative regulators to reduce H3K36me2 and H3K36me3 on wild type histone H3 [95][96][97][98]. H3K36M oncohistones reduces H3K36me2 and H3K36me3 genome-wide through the inhibition of at least two histone H3K36 methyltransferases, NSD2 and SETD2 [96][97][98][99]. Knock-in of heterozygous H3.3K36M mutation into chondrocytes reduces the H3K36 methylation and subsequent expression of cancer related genes.…”

Section: H3k36me3 Associated Ddr In Tumorigenesismentioning

confidence: 99%

“…Indeed, H3K27me3 increases in the intergenic regions where the H3K36me2 is decreased in the H3.3K36M mutate cells [97,98]. How this H3K36M mutation controls DNA damage repair is still unknown [94,99]. More efforts should be placed to discover the detailed molecular mechanisms of how oncohistones promote tumorigenesis through DNA damage repair pathways.…”

Section: H3k36me3 Associated Ddr In Tumorigenesismentioning

confidence: 99%

H3K36me3, message from chromatin to DNA damage repair

et al. 2020

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Histone marks control many cellular processes including DNA damage repair. This review will focus primarily on the active histone mark H3K36me3 in the regulation of DNA damage repair and the maintenance of genomic stability after DNA damage. There are diverse clues showing H3K36me3 participates in DNA damage response by directly recruiting DNA repair machinery to set the chromatin at a "ready" status, leading to a quick response upon damage. Reduced H3K36me3 is associated with low DNA repair efficiency. This review will also place a main emphasis on the H3K36me3-mediated DNA damage repair in the tumorigenesis of the newly found oncohistone mutant tumors. Gaining an understanding of different aspects of H3K36me3 in DNA damage repair, especially in cancers, would share the knowledge of chromatin and DNA repair to serve to the drug discovery and patient care.

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“…The delay in replication may partly explain the profile, although the mechanism remains unknown. Unlike H3K4 methylation, H3K36me2 and H3K36me3 localized broadly to euchromatin and gene body, respectively (Li et al, 2019;Zee et al, 2010b), and the replication timing of chromatin that harbors these modifications may not be as early as that of H3K4-associated chromatin. Since H3K27 is reportedly methylated (H3K27me1) in combination with H3K36 (Zheng et al, 2016), its dynamics may be similar to H3K36 methylation.…”

mentioning

confidence: 99%

Histone modification dynamics as revealed by a multicolor immunofluorescence-based single-cell analysis

Hayashi‐Takanaka

Kina

Nakamura

et al. 2020

Preprint

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Post-translational modifications on histones can be stable epigenetic marks and transient signals that can occur in response to internal and external stimuli. Levels of histone modifications fluctuate during the cell cycle and vary among different cell types. Here we describe a simple system to monitor the levels of multiple histone modifications in single cells by multicolor immunofluorescence using directly labeled modification-specific antibodies. We first analyzed histone H3 and H4 modifications during the cell cycle. Levels of active marks, such as acetylation and H3K4 methylation, were increased during the S phase, in association with chromatin duplication. By contrast, levels of some repressive modifications gradually increased during the G2 and the next G1 phases. We applied this method to validate the target modifications of various histone demethylases in cells using a transient overexpression system. We also screened chemical compounds in marine organism extracts that affect histone modifications and identified psammaplin A, which was previously reported to inhibit histone deacetylases. Thus, the method presented here is a powerful and convenient tool for analyzing the changes in histone modifications.

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Understanding histone H3 lysine 36 methylation and its deregulation in disease

Cited by 111 publications

References 174 publications

ASH1L REGULATES THE STRUCTURAL DEVELOPMENT OF NEURONAL CIRCUITRY BY MODULATING BDNF/TrkB SIGNALING IN HUMAN NEURONS

ASH1L REGULATES THE STRUCTURAL DEVELOPMENT OF NEURONAL CIRCUITRY BY MODULATING BDNF/TrkB SIGNALING IN HUMAN NEURONS

H3K36me3, message from chromatin to DNA damage repair

Histone modification dynamics as revealed by a multicolor immunofluorescence-based single-cell analysis

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