Abstract
Inhibition of cell division is an active response to DNA damage that enables cells to maintain genome integrity. However, how DNA damage arrests the plant cell cycle is largely unknown. Here, we show that the repressor-type R1R2R3-Myb transcription factors (Rep-MYBs), which suppress G2/M-specific genes, are required to inhibit cell division in response to DNA damage. Knockout mutants are resistant to agents that cause DNA double-strand breaks and replication stress. Cyclin-dependent kinases (CDKs) can phosphorylate Rep-MYBs in vitro and are involved in their proteasomal degradation. DNA damage reduces CDK activities and causes accumulation of Rep-MYBs and cytological changes consistent with cell cycle arrest. Our results suggest that CDK suppressors such as CDK inhibitors are not sufficient to arrest the cell cycle in response to DNA damage but that Rep-MYB-dependent repression of G2/M-specific genes is crucial, indicating an essential function for Rep-MYBs in the DNA damage response.
Highlights
Inhibition of cell division is an active response to DNA damage that enables cells to maintain genome integrity
The DNA damage checkpoint is triggered by the sensor kinases ATM and ATR (ATM-related and Rad3related); ATM senses DNA double-strand breaks (DSBs), while ATR is primarily activated by replication stress and single-strand breaks (SSBs)[5, 6]
We previously reported that DSBs increase the expression of Cyclin-dependent kinases (CDKs) suppressors, such as CDK inhibitors, and downregulate cyclin A (CYCA) and B (CYCB) genes, which are essential for CDK activation at G2/M14
Summary
This result agrees with data obtained from zeocin-treated cultured cells[14]. Since Rep-MYBs did not respond to zeocin at the mRNA level, we observed protein accumulation of MYB3R3 using ProMYB3R3::MYB3R3-GFP, which carries the 1.3-kb promoter and the protein-coding region of MYB3R3. This reporter gene can complement the myb3r3 mutation, indicating that the MYB3R3GFP fusion protein is functional[20]. GFP signals were very faint in the absence of zeocin, but became pronounced in the meristem after 12 h of zeocin treatment and thereafter (Fig. 2a).
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