ArticleNucleic acids research2016
Chromosome territory relocation during DNA repair requires nuclear myosin 1 recruitment to chromatin mediated by ϒ-H2AX signaling.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 60 citations in OpenAlex.
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- Regulation of Nuclear Mechanics and the Impact on DNA Damage.International journal of molecular sciences · 2021Review
- Journey to the Center of the Cell: Cytoplasmic and Nuclear Actin in Immune Cell Functions.Frontiers in cell and developmental biology · 2021Review
- Elevated HNF1A expression promotes radiation-resistance via driving PI3K/AKT signaling pathway in esophageal squamous cell carcinoma cells.Journal of Cancer · 2021Article
- Interphase Chromosomes in Replicative Senescence: Chromosome Positioning as a Senescence Biomarker and the Lack of Nuclear Motor-Driven Chromosome Repositioning in Senescent Cells.Frontiers in cell and developmental biology · 2021Article
- Modulation of DNA double-strand break repair as a strategy to improve precise genome editing.Oncogene · 2020Review
- Nuclear myosin 1 activates p21 gene transcription in response to DNA damage through a chromatin-based mechanism.Communications biology · 2020Article
- Complex Chromatin Motions for DNA Repair.Frontiers in genetics · 2020Review
- Radial Organization in the Mammalian Nucleus.Frontiers in genetics · 2020Review
- Nuclear actin filaments in DNA repair dynamics.Nature cell biology · 2019Review
- Actin' between phase separated domains for heterochromatin repair.DNA repair · 2019Review
- Lamin A/C and Emerin depletion impacts chromatin organization and dynamics in the interphase nucleus.BMC molecular and cell biology · 2019Article
- Maintenance of epigenetic landscape requires CIZ1 and is corrupted in differentiated fibroblasts in long-term culture.Nature communications · 2019Article
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
During DNA damage response (DDR), certain gene rich chromosome territories (CTs) relocate to newer positions within interphase nuclei and revert to their native locations following repair. Such dynamic relocation of CTs has been observed under various cellular conditions, however, the underlying mechanistic basis of the same has remained largely elusive. In this study, we aim to understand the temporal and molecular details of such crosstalk between DDR signaling and CT relocation dynamics. We demonstrate that signaling at DNA double strand breaks (DSBs) by the phosphorylated histone variant (ϒ-H2AX) is a pre-requisite for damage induced CT relocation, as cells deficient in ϒ-H2AX signaling fail to exhibit such a response. Inhibition of Rad51 or DNA Ligase IV mediated late steps of double strand break repair does not seem to abrogate CT relocation completely. Upon DNA damage, an increase in the levels of chromatin bound motor protein nuclear myosin 1 (NM1) ensues, which appears to be functionally linked to ϒ-H2AX signaling. Importantly, the motor function of NM1 is essential for its recruitment to chromatin and CT relocation following damage. Taking these observations together, we propose that early DDR sensing and signaling result in NM1 recruitment to chromosomes which in turn guides DNA damage induced CT relocation.
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