Abstract
Cell cycle arrest is an active response to stresses that enables organisms to survive under fluctuating environmental conditions. While signalling pathways that inhibit cell cycle progression have been elucidated, the putative core module orchestrating cell cycle arrest in response to various stresses is still elusive. Here we report that in Arabidopsis, the NAC-type transcription factors ANAC044 and ANAC085 are required for DNA damage-induced G2 arrest. Under genotoxic stress conditions, ANAC044 and ANAC085 enhance protein accumulation of the R1R2R3-type Myb transcription factor (Rep-MYB), which represses G2/M-specific genes. ANAC044/ANAC085-dependent accumulation of Rep-MYB and cell cycle arrest are also observed in the response to heat stress that causes G2 arrest, but not to osmotic stress that retards G1 progression. These results suggest that plants deploy the ANAC044/ANAC085-mediated signalling module as a hub which perceives distinct stress signals and leads to G2 arrest.
Highlights
To survive under fluctuating environmental conditions, all organisms have the ability to deal with various kinds of internal and external stresses
Phylogenetic analysis of NAC transcription factors indicated that ANAC044 and ANAC085 are the closest relatives of SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) (Figure 1A); in the NAC domain, which is essential for DNA binding, their amino acid similarity to SOG1 is 72.0% for ANAC044 and 72.6% for ANAC085
Note that the MYB3R3 transcript level was unaltered by mutations in SOG1, ANAC044 or ANAC085 (Figure 6—figure supplement 1). These results suggest that ANAC044 and ANAC085 as well as SOG1 are involved in DNA damage-induced accumulation of the repressor-type MYB3Rs
Summary
To survive under fluctuating environmental conditions, all organisms have the ability to deal with various kinds of internal and external stresses. A recent report demonstrated that Rep-MYBs function as major repressors of cell cycle genes in the response to DNA damage (Bourbousse et al, 2018) It remains unknown whether the initial reduction of CDK activity is sufficient to trigger Rep-MYB stabilization, or whether another signalling pathway is required to accumulate a sufficient amount of Rep-MYB for the suppression of numerous G2/M-specific genes. ANAC044 and ANAC085 are not required for the induction of genes for DNA repair proteins or CDK inhibitors, but rather are engaged in accumulation of Rep-MYBs. Our data show that they participate in heat stressinduced inhibition of G2 progression, suggesting that an ANAC044- and ANAC085-mediated pathway plays a central role in orchestrating stress-induced G2 arrest by controlling Rep-MYB accumulation
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