DNA-translocation-independent role of INO80 remodeler in DNA damage repairs

Sokolova, Vladyslava; Lee, Gahyun; Mullins, Amber; Mody, Preesha; Watanabe, Shinya; Tan, Dongyan

doi:10.1016/j.jbc.2023.105245

Cited by 3 publications

(3 citation statements)

References 42 publications

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“…If nuclear actin polymerization reduces the availability of G-actin, the stability of these chromatin-modifying complexes might be decreased. Importantly, these actin monomerbinding complexes might affect DNA repair, as was shown, for example, for TIP60 and INO80 [60][61][62][63][64][65].…”

Section: Nuclear Actin Polymerization Promotes Dna Repair By Hrmentioning

confidence: 80%

Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?

He,

Brakebusch

2024

Cells

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Although more difficult to detect than in the cytoplasm, it is now clear that actin polymerization occurs in the nucleus and that it plays a role in the specific processes of the nucleus such as transcription, replication, and DNA repair. A number of studies suggest that nuclear actin polymerization is promoting precise DNA repair by homologous recombination, which could potentially be of help for precise genome editing and gene therapy. This review summarizes the findings and describes the challenges and chances in the field.

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Section: Nuclear Actin Polymerization Promotes Dna Repair By Hrmentioning

confidence: 80%

Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?

He,

Brakebusch

2024

Cells

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“…Like other members of the chromatin remodeler superfamily, INO80 exhibits typical remodeling activities such as mobilizing nucleosomes locally and influencing nucleosome spacing in vivo [ 44 , 45 ]. These functions are attributed to the enzyme’s capacity to reposition nucleosomes along DNA in an ATP-dependent manner [ 46 ]. Notably, H2A.Z nucleosomes are recognized as better substrates for INO80 compared to canonical nucleosomes in a nucleosome-sliding assay [ 47 ].…”

Section: Resultsmentioning

confidence: 99%

Structural and Biochemical Characterization of the Nucleosome Containing Variants H3.3 and H2A.Z

Jung,

Sokolova,

Lee

et al. 2024

Epigenomes

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Variant H3.3, along with H2A.Z, is notably enriched at promoter regions and is commonly associated with transcriptional activation. However, the specific molecular mechanisms through which H3.3 influences chromatin dynamics at transcription start sites, and its role in gene regulation, remain elusive. Using a combination of biochemistry and cryo-electron microscopy (cryo-EM), we show that the inclusion of H3.3 alone does not induce discernible changes in nucleosome DNA dynamics. Conversely, the presence of both H3.3 and H2A.Z enhances DNA’s flexibility similarly to H2A.Z alone. Interestingly, our findings suggest that the presence of H3.3 in the H2A.Z nucleosome provides slightly increased protection to DNA at internal sites within the nucleosome. These results imply that while H2A.Z at active promoters promotes the formation of more accessible nucleosomes with increased DNA accessibility to facilitate transcription, the simultaneous presence of H3.3 offers an additional mechanism to fine-tune nucleosome accessibility and the chromatin environment.

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“…ATPase-dependent chromatin-remodeling complexes are associated with the occurrence and development of coronary heart disease, heart failure, pathological myocardial hypertrophy, and other cardiovascular diseases. Although there are few studies on the regulation of ATP-dependent nucleosome chromatin remodeling complexes in cardiovascular diseases, they are rich in research fields such as malignant tumors, lipid metabolism, immune regulation, DNA damage and repair, and autophagy [ 158 – 161 ]. For example, the SWI/SNF complex contains multiple subunits, and different subunits drive the occurrence of different diseases.…”

Section: Types Of Chromatin Modifiersmentioning

confidence: 99%

Chromatin modifiers in human disease: from functional roles to regulatory mechanisms

Nie,

Song,

Huang

et al. 2024

Mol Biomed

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The field of transcriptional regulation has revealed the vital role of chromatin modifiers in human diseases from the beginning of functional exploration to the process of participating in many types of disease regulatory mechanisms. Chromatin modifiers are a class of enzymes that can catalyze the chemical conversion of pyrimidine residues or amino acid residues, including histone modifiers, DNA methyltransferases, and chromatin remodeling complexes. Chromatin modifiers assist in the formation of transcriptional regulatory circuits between transcription factors, enhancers, and promoters by regulating chromatin accessibility and the ability of transcription factors to acquire DNA. This is achieved by recruiting associated proteins and RNA polymerases. They modify the physical contact between cis-regulatory factor elements, transcription factors, and chromatin DNA to influence transcriptional regulatory processes. Then, abnormal chromatin perturbations can impair the homeostasis of organs, tissues, and cells, leading to diseases. The review offers a comprehensive elucidation on the function and regulatory mechanism of chromatin modifiers, thereby highlighting their indispensability in the development of diseases. Furthermore, this underscores the potential of chromatin modifiers as biomarkers, which may enable early disease diagnosis. With the aid of this paper, a deeper understanding of the role of chromatin modifiers in the pathogenesis of diseases can be gained, which could help in devising effective diagnostic and therapeutic interventions.

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DNA-translocation-independent role of INO80 remodeler in DNA damage repairs

Cited by 3 publications

References 42 publications

Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?

Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?

Structural and Biochemical Characterization of the Nucleosome Containing Variants H3.3 and H2A.Z

Chromatin modifiers in human disease: from functional roles to regulatory mechanisms

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