Repair of single-strand breaks during the cell cycle - saturation of repair capacity

Imaging of recruitment of XRCC1 and PCNA to a predetermined number of DNA single-strand breaks (SSB) demonstrates that (i) short-patch base excision repair is active throughout the whole cell cycle and repairs SSBs in over 60% of nonreplicating cells, while long-patch BER is active in approximately 30% of nonreplicating cells, becomes inactive in the early S phase and shows activity again in the mid and late S phase (in 8 and 16% of cells, respectively), (ii) cells retain the capacity to respond to damage if the total number of SSBs induced within seconds does not exceed approximately 110, more breaks evoke no XRCC1 recruitment; (iii) within less than a second, a cell commits a part of the currently available pool of XRCC1 molecules to accumulation at the damage site. We hypothesize that a limit on the number of single-strand breaks that elicit the BER response can arise from limited poly-ADP-ribosylation.

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Publication Details

Journal
Nucleus
Published
2026-05-17
DOI
https://doi.org/10.1080/19491034.2026.2673717
Primary Topic
DNA Repair Mechanisms
Type
article
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article

Repair of single-strand breaks during the cell cycle - saturation of repair capacity

Agnieszka Hoang-Bujnowicz, Oskar Szelest, Mirosław Zarębski, Jurek W. Dobrucki
Nucleus
DNA Repair Mechanisms
article

Repair of single-strand breaks during the cell cycle - saturation of repair capacity

Agnieszka Hoang-Bujnowicz, Oskar Szelest, Mirosław Zarębski, Jurek W. Dobrucki
article en

Abstract

Imaging of recruitment of XRCC1 and PCNA to a predetermined number of DNA single-strand breaks (SSB) demonstrates that (i) short-patch base excision repair is active throughout the whole cell cycle and repairs SSBs in over 60% of nonreplicating cells, while long-patch BER is active in approximately 30% of nonreplicating cells, becomes inactive in the early S phase and shows activity again in the mid and late S phase (in 8 and 16% of cells, respectively), (ii) cells retain the capacity to respond to damage if the total number of SSBs induced within seconds does not exceed approximately 110, more breaks evoke no XRCC1 recruitment; (iii) within less than a second, a cell commits a part of the currently available pool of XRCC1 molecules to accumulation at the damage site. We hypothesize that a limit on the number of single-strand breaks that elicit the BER response can arise from limited poly-ADP-ribosylation.

NucleusVol. 17(1)
Jagiellonian University (PL)
Openalex Percentile: Top 9%
DNA Repair Mechanisms
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