AI Article Synopsis

  • Chromosomal locations become more mobile in response to DNA double-strand breaks during both S phase and G1 phase, indicating an adaptive response to DNA damage.
  • The mechanisms behind this mobility are regulated by the DNA damage checkpoint and recombination proteins like Rad51, suggesting a critical role in locating repair templates.
  • This study reveals that homologous recombination may take place during G1 phase, challenging previous beliefs that such processes only occur in S phase.

Article Abstract

During S phase in , chromosomal loci become mobile in response to DNA double-strand breaks both at the break site (local mobility) and throughout the nucleus (global mobility). Increased nuclear exploration is regulated by the recombination machinery and the DNA damage checkpoint and is likely an important aspect of homology search. While mobility in response to DNA damage has been studied extensively in S phase, the response in interphase has not, and the question of whether homologous recombination proceeds to completion in G1 phase remains controversial. Here, we find that global mobility is triggered in G1 phase. As in S phase, global mobility in G1 phase is controlled by the DNA damage checkpoint and the Rad51 recombinase. Interestingly, despite the restriction of Rad52 mediator foci to S phase, Rad51 foci form at high levels in G1 phase. Together, these observations indicate that the recombination and checkpoint machineries promote global mobility in G1 phase, supporting the notion that recombination can occur in interphase diploids.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6761769PMC
http://dx.doi.org/10.1091/mbc.E19-08-0469DOI Listing

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