To cope with DNA damage, proliferating cells have evolved sophisticated mechanisms including cell cycle arrest and activation of DNA repair. Paradoxically, various DNA damage response pathways are promoted by cyclin‐dependent kinase (CDK) activity, while cell cycle remains arrested. New work in The EMBO Journal shows that plant cells have evolved intricate ways to resolve this dilemma, by utilizing distinct and specialized CDKs for cell cycle progression and homologous recombination.
See also: AK Weimer et al (October 2016)
The cell division cycle consists of a unidirectional series of highly coordinated events that end up in the production of two daughter cells. Its main driving force is the activity of various cyclin/CDK complexes, allowing cells to progress from G1 into S phase, through S phase, and in G2 phase enabling chromosome segregation during mitosis. Unidirectional progression is achieved by fluctuations in CDK activity, which results from a sophisticated regulatory balance involving primarily cyclical accumulation and timely degradation of their cyclin subunits, the presence of CDK inhibitors, and the action of CDK‐activating or CDK‐inhibiting kinases and phosphatases. In addition to normal cell cycle progression, the unavoidable occurrence of various types of DNA damage either resulting from normal cellular physiology or from attack by a plethora of exogenous DNA‐damaging agents requires a fast and precise response of the proliferating cell.
The cellular response to the presence of DNA damage is of fundamental importance to prevent the accumulation of DNA lesions, the occurrence of chromosomal replication and segregation errors, and the transmission of mutated genomes to daughter cells. Briefly, such cellular responses include (i) various complementary mechanisms for immediate cell cycle arrest to prevent cell division with damaged DNA, (ii) activation of appropriate DNA repair pathways to fix the DNA damage in a highly lesion‐specific manner, and (iii) activation of DNA damage tolerance pathways.
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