AI Article Synopsis
- CDKs are usually inhibited during DNA damage to stop cell division, but they are necessary for DNA repair, particularly homology-dependent repair (HR).
- Researchers discovered that Arabidopsis thaliana uses a "division of labor" approach, where B1-type CDKs and cyclins are key players in HR.
- Specifically, CDKB1-CYCB1 complexes activate RAD51, a crucial protein for DNA repair, after DNA damage, while mitotic cell-cycle activity is still blocked.
Article Abstract
Upon DNA damage, cyclin-dependent kinases (CDKs) are typically inhibited to block cell division. In many organisms, however, it has been found that CDK activity is required for DNA repair, especially for homology-dependent repair (HR), resulting in the conundrum how mitotic arrest and repair can be reconciled. Here, we show that Arabidopsis thaliana solves this dilemma by a division of labor strategy. We identify the plant-specific B1-type CDKs (CDKB1s) and the class of B1-type cyclins (CYCB1s) as major regulators of HR in plants. We find that RADIATION SENSITIVE 51 (RAD51), a core mediator of HR, is a substrate of CDKB1-CYCB1 complexes. Conversely, mutants in CDKB1 and CYCB1 fail to recruit RAD51 to damaged DNA CYCB1;1 is specifically activated after DNA damage and we show that this activation is directly controlled by SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a transcription factor that acts similarly to p53 in animals. Thus, while the major mitotic cell-cycle activity is blocked after DNA damage, CDKB1-CYCB1 complexes are specifically activated to mediate HR.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5048351 | PMC |
| http://dx.doi.org/10.15252/embj.201593083 | DOI Listing |
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