A plant solution to the CDK conundrum in the DNA damage response

Abstract

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.

Figure 1. Summary of the major DNA damage response pathways in plant cells

After sensing damage such as DSBs, an ATR‐dependent pathway contributes to cell cycle arrest by inhibiting CDK/cyclin complexes needed for the G2/M transition. Concomitantly, an ATM‐dependent pathway upregulates the plant‐specific transcription factor SOG1 that activates expression of hundreds of genes, including the CDK inhibitors SMR5 and SMR7, genes required for entering and progressing through the endocycle program, and CYCB1. CYCB1 together with the plant‐specific CDKB1 phosphorylates RAD51 to promote HR repair. Meanwhile, the key cell cycle CDK activity remains suppressed solving the dilemma of conflicting CDK regulation requirements in response to DNA damage.