ATM‐mediated phosphorylation of SOG1 is essential for the DNA damage response in Arabidopsis

Abstract

Arabidopsis SOG1 (suppressor of gamma response 1) is a plantspecific transcription factor that governs the DNA damage response. Here we report that SOG1 is phosphorylated in response to DNA damage, and that this phosphorylation is mediated by the sensor kinase ataxia telangiectasia mutated (ATM). We show that SOG1 phosphorylation is crucial for the response to DNA damage, including transcriptional induction of downstream genes, transient arrest of cell division and programmed cell death. Although the amino-acid sequences of SOG1 and the mammalian tumour suppressor p53 show no similarity, this study demonstrates that ATM-mediated phosphorylation of a transcription factor has a pivotal role in the DNA damage response in both plants and mammals.

SUPPRESSOR OF GAMMA RESPONSE1 Links DNA Damage Response to Organ Regeneration

“…We also demonstrate that SOG1 is required for the arrest of the cell cycle in these surviving cells, also within 6 to 10 h after IR. This arrest, along with the previously reported role of SOG1 in the induction DNA repair transcripts (Culligan et al, 2006;Yoshiyama et al, 2013), can support the mitotic competency of remnant cells that are needed to replenish the IR-compromised SCN and hence resume growth. sog1 mutants' defect in cell cycle arrest (8 h), along with their failed induction of DNA repair transcripts (Yoshiyama et al, 2013), predisposes them to the (32 h onset) cell death seen across the root's mitotic zone in all cell types.…”

“…This arrest, along with the previously reported role of SOG1 in the induction DNA repair transcripts (Culligan et al, 2006;Yoshiyama et al, 2013), can support the mitotic competency of remnant cells that are needed to replenish the IR-compromised SCN and hence resume growth. sog1 mutants' defect in cell cycle arrest (8 h), along with their failed induction of DNA repair transcripts (Yoshiyama et al, 2013), predisposes them to the (32 h onset) cell death seen across the root's mitotic zone in all cell types. A similar (patchy) pattern of IR-induced cell death across the mitotic zone was also demonstrated in atr, atm double mutants (Furukawa et al, 2010).…”

“…It is unlikely that the loss of the QC markers was due to the death of QC cells, as they are particularly resistant to IR-induced cell death (Curtis and Hays, 2007;Heyman et al, 2013), in contrast to the cells that surround the QC ( Fig. 1C; Furukawa et al, 2010;Yoshiyama et al, 2013).…”

“…ATM (Yoshiyama et al, 2013) and inferably ATR (Furukawa et al, 2010;Yoshiyama et al, 2009) can phosphoactivate the transcription factor SOG1, as well as other proteins, in plant cells (Roitinger et al, 2015;Yoshiyama et al, 2013). Once activated, SOG1 transcriptionally induces various functional classes of DDR genes (Yoshiyama et al, 2009;Missirian et al, 2014;Ricaud et al, 2007); SOG1 induces a robust set of .100 transcripts by $4-fold within 1.5 h in response to 100 Gy IR (Culligan et al, 2006;Furukawa et al, 2010).…”

SOG1: a master regulator of the DNA damage response in plants

“…Furthermore, neither cell death of root stem cells nor endoreduplication of root epidermal and cortex cells is observed in the sog1-1 mutant upon treatment with DNA-damaging agents (Furukawa et al, 2010;Adachi et al, 2011). Thus, SOG1 contributes to the maintenance of genome stability after DNA damage by inducing several pathways, including cell cycle arrest, Yoshiyama et al (2013), reproduced with permission.) SOG1 is a master regulator of the DDR in plants DNA repair, programmed cell death and endoreduplication, through the regulation of many genes.…”