Histone Variant H3.3: A versatile H3 variant in health and in disease

Xiong, Cong; Wen, Zengqi; Li, Guohong

doi:10.1007/s11427-016-5006-9

Cited by 6 publications

(2 citation statements)

References 88 publications

(116 reference statements)

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“…Histone chaperones are essential in the regulation of histone dynamics, genome stability and cell identity [ 6 ]. The incorporation of histone variants may create architecturally distinct chromatin regions by regulating the structure and dynamics of chromatin fibers, which enables the chromatin to play diverse functions in chromatin-associated processes [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

UBN1/2 of HIRA complex is responsible for recognition and deposition of H3.3 at cis-regulatory elements of genes in mouse ES cells

Xiong

Wen

et al. 2018

BMC Biol

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BackgroundH3.3 is an ancient and conserved H3 variant and plays essential roles in transcriptional regulation. HIRA complex, which is composed of HIRA, UBN1 or UBN2, and Cabin1, is a H3.3 specific chaperone complex. However, it still remains largely uncharacterized how HIRA complex specifically recognizes and deposits H3.3 to the chromatin, such as promoters and enhancers.ResultsIn this study, we demonstrate that the UBN1 or UBN2 subunit is mainly responsible for specific recognition and direct binding of H3.3 by the HIRA complex. While the HIRA subunit can enhance the binding affinity of UBN1 toward H3.3, Cabin1 subunit cannot. We also demonstrate that both Ala87 and Gly90 residues of H3.3 are required and sufficient for the specific recognition and binding by UBN1. ChIP-seq studies reveal that two independent HIRA complexes (UBN1-HIRA and UBN2-HIRA) can cooperatively deposit H3.3 to cis-regulatory regions, including active promoters and active enhancers in mouse embryonic stem (mES) cells. Importantly, disruption of histone chaperone activities of UBN1 and UBN2 by FID/AAA mutation results in the defect of H3.3 deposition at promoters of developmental genes involved in neural differentiation, and subsequently causes the failure of activation of these genes during neural differentiation of mES cells.ConclusionTogether, our results provide novel insights into the mechanism by which the HIRA complex specifically recognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.Electronic supplementary materialThe online version of this article (10.1186/s12915-018-0573-9) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

UBN1/2 of HIRA complex is responsible for recognition and deposition of H3.3 at cis-regulatory elements of genes in mouse ES cells

Xiong

Wen

et al. 2018

BMC Biol

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“…Under some conditions, these alterations are associated with myocardial regenerative processes. For instance, the substitution of histone 3 (H3) with histone variant H3.3 in proliferating cardiomyocytes resulted in faulty DNA repair and SASP phenotypes [ 187 ]. Meanwhile, H3 replacement with another histone variant, histone H3-like centromeric protein A (CENPA), is crucial for kinetochore formation and function during cell division [ 188 ].…”

Section: Introductionmentioning

confidence: 99%

Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets

Luan,

Zhu,

Jiao

et al. 2024

Cell Death Discov.

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Cardiac aging, particularly cardiac cell senescence, is a natural process that occurs as we age. Heart function gradually declines in old age, leading to continuous heart failure, even in people without a prior history of heart disease. To address this issue and improve cardiac cell function, it is crucial to investigate the molecular mechanisms underlying cardiac senescence. This review summarizes the main mechanisms and key proteins involved in cardiac cell senescence. This review further discusses the molecular modulators of cellular senescence in aging hearts. Furthermore, the discussion will encompass comprehensive descriptions of the key drugs, modes of action and potential targets for intervention in cardiac senescence. By offering a fresh perspective and comprehensive insights into the molecular mechanisms of cardiac senescence, this review seeks to provide a fresh perspective and important theoretical foundations for the development of drugs targeting this condition.

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Challenges for base excision repair enzymes: Acquiring access to damaged DNA in chromatin

Delaney

2019

DNA Repair

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Histone Variant H3.3: A versatile H3 variant in health and in disease

Cited by 6 publications

References 88 publications

UBN1/2 of HIRA complex is responsible for recognition and deposition of H3.3 at cis-regulatory elements of genes in mouse ES cells

UBN1/2 of HIRA complex is responsible for recognition and deposition of H3.3 at cis-regulatory elements of genes in mouse ES cells

Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets

Challenges for base excision repair enzymes: Acquiring access to damaged DNA in chromatin

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