Nuclear Actin and Actin-Binding Proteins in DNA Repair

Hurst, Verena; Shimada, Kenji; Gasser, Susan M.

doi:10.1016/j.tcb.2019.02.010

Cited by 115 publications

(84 citation statements)

References 132 publications

(206 reference statements)

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“…Akin to transcription, multiple factors contribute to chromatin motion. The degree to which movement reflects intrinsic changes to the chromatin fiber (e.g., by chromatin remodeling complexes) or extrinsic forces applied to chromatin (e.g., IDPs and the nuclear cytoskeleton) is a subject of rigorous study and debate ( Hurst et al, 2019 ). A functional role for the actin-nucleating Arp2/3 complex has emerged as a driver of large-scale chromosomal movements during DSB repair.…”

Section: Nuclear Domains: Organizing Genomic Transactionsmentioning

confidence: 99%

Assembling nuclear domains: Lessons from DNA repair

Schrank

Gautier

2019

Journal of Cell Biology

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Eukaryotic nuclei are organized into nuclear domains that unite loci sharing a common function. These domains are essential for diverse processes including (1) the formation of topologically associated domains (TADs) that coordinate replication and transcription, (2) the formation of specialized transcription and splicing factories, and (3) the clustering of DNA double-strand breaks (DSBs), which concentrates damaged DNA for repair. The generation of nuclear domains requires forces that are beginning to be identified. In the case of DNA DSBs, DNA movement and clustering are driven by actin filament nucleators. Furthermore, RNAs and low-complexity protein domains such as RNA-binding proteins also accumulate around sites of transcription and repair. The link between liquid–liquid phase separation and actin nucleation in the formation of nuclear domains is still unknown. This review discusses DSB repair domain formation as a model for functional nuclear domains in other genomic contexts.

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Section: Nuclear Domains: Organizing Genomic Transactionsmentioning

confidence: 99%

Assembling nuclear domains: Lessons from DNA repair

Schrank

Gautier

2019

Journal of Cell Biology

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“…ACTR3B, also known as actin related protein 3B, had implications in the nucleation and assembly of branched actin networks [30]. It bound to DNA double-strand fractures and, in conjunction with actin, facilitating clustering and homologous directed repair at the breakage [31]. There was evidence that the disturbance in ACTR3B expression was account for abnormal neuronal morphology and synaptic growth, as well as alterations in synapse activity [32][33][34], which was likely related to the pathogenesis of early death in HD.…”

Section: Discussionmentioning

confidence: 99%

Regulatory network underlying alterations of gene expression in early death of Huntington's disease

Zhou¹,

Chen²,

Zhong³

et al. 2020

Preprint

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The aim of this study is to explore the genomic mechanism of early death in Huntington’s disease (HD). We identified 10160 and 1511 differentially expressed genes (DEGs) from comparisons of HD versus control and early versus late death, respectively. On the basis of 922 overlapped DEGs among them, six functional modules were established by weight gene correlation network analysis. The turquoise module most strongly related to overall survival of HD was significantly enriched in GABAergic synapse, retrograde endocannabinoid signaling and neuroactive ligand-receptor interaction. Low expression of five DEGs (CA10, WSB2, ACTR3B, PCDH19 and GABRB3) with highest degree of connectivity and non-zero regression coefficients were identified as hub genes, based on which the LASSO model exactly predicted the occurrence of early death in HD. Furthermore, the network analysis revealed indirect interaction of CA10 with the central hub gene GABRB3, which was involved in the pathway of GABAergic synapse. Compared with high expression of hub genes, their low expression appeared shorter overall survival of HD patients according to Kaplan-Meier survival analysis. Consequently, low expression of CA10, WSB2, ACTR3B, PCDH19 and GABRB3 were possibly associated with early death of HD. The likelihood of low expression of GABRB3 regulated by CA10 in GABAergic synapse contributed to the pathogenesis of early death in HD.

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“… Actin and ABPs in cancer cells invasion and migration. Modified on the basis of Winder and Ayscough (2005) and Hurst et al (2019) [ 5 , 124 ]. …”

Section: Figurementioning

confidence: 99%

Involvement of Actin and Actin-Binding Proteins in Carcinogenesis

Izdebska

Zielińska

Hałas‐Wiśniewska

et al. 2020

Cells

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The actin cytoskeleton plays a crucial role in many cellular processes while its reorganization is important in maintaining cell homeostasis. However, in the case of cancer cells, actin and ABPs (actin-binding proteins) are involved in all stages of carcinogenesis. Literature has reported that ABPs such as SATB1 (special AT-rich binding protein 1), WASP (Wiskott-Aldrich syndrome protein), nesprin, and villin take part in the initial step of carcinogenesis by regulating oncogene expression. Additionally, changes in actin localization promote cell proliferation by inhibiting apoptosis (SATB1). In turn, migration and invasion of cancer cells are based on the formation of actin-rich protrusions (Arp2/3 complex, filamin A, fascin, α-actinin, and cofilin). Importantly, more and more scientists suggest that microfilaments together with the associated proteins mediate tumor vascularization. Hence, the presented article aims to summarize literature reports in the context of the potential role of actin and ABPs in all steps of carcinogenesis.

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Nuclear Actin and Actin-Binding Proteins in DNA Repair

Cited by 115 publications

References 132 publications

Assembling nuclear domains: Lessons from DNA repair

Assembling nuclear domains: Lessons from DNA repair

Regulatory network underlying alterations of gene expression in early death of Huntington's disease

Involvement of Actin and Actin-Binding Proteins in Carcinogenesis

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