SUPPRESSOR OF GAMMA RESPONSE1 Links DNA Damage Response to Organ Regeneration

A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis

“…In WT roots, PI-stained dead cells derived from stem cells and stele precursor cells gradually decreased and almost disappeared within five days (Figure 3-figure supplement 4). In sog1-101 , stem cell death did not occur, although we observed sporadic cell death across the meristematic zone and distorted tissue organization (Figure 3-figure supplement 4), which were also described by Johnson et al (2018). On the other hand, anac044-1 anac085-1 displayed no cell death in the stem cell niche or in the meristematic zone, and cells were properly arranged in the root tip throughout 7 days after recovery (Figure 3-figure supplement 4).…”

Suppressor of Gamma Response 1 Modulates the DNA Damage Response and Oxidative Stress Response in Leaves of Cadmium-Exposed Arabidopsis thaliana

“…Root meristem size was decreased in WT roots exposed to zeocin, whereas this effect was not observed in sog1-1 mutant roots, indicating that SOG1 is required for the zeocininduced early onset of endoreplication (Chen and Umeda, 2015). A similar result was described by Johnson et al (2018), showing that the inhibition of DNA replication and cell division observed in the mitotic zone of WT roots shortly after exposure to ionizing radiation was absent in sog1-1 mutants. Our data indicate that the Cd-induced inhibition of endoreplication in WT plants is also absent in the sog1-7 mutants (Figure 2), suggesting that under these stress conditions, SOG1 is responsible for the inhibition rather than activation of endoreplication.…”

“…This SOG1-mediated cell death causes the removal of a subset of stem cells and induces a regeneration response in the surrounding root apical meristem. As a consequence, a functional stem cell niche is regained, enabling continued root growth (Johnson et al, 2018). A similar mechanism might be induced by SOG1 upon Cd exposure, as Cd was also shown to induce cell death in the root meristem of Pisum sativum (Lehotai et al, 2011) and A. cepa (Behboodi and Samadi, 2004).…”

AtCAF‐1 mutants show different DNA damage responses after ultraviolet‐B than those activated by other genotoxic agents in leaves

“…Interestingly, primary root elongation was significantly more inhibited by UV‐B in fas1 and fas2 than in WT plants (Figure c and Figure S5). Previously, Johnson et al () showed that in roots, the programmed destruction of the mitotically compromised stem cell niche after DNA damage triggers its regeneration, enabling growth recovery. Thus, to analyze if the higher decrease in root elongation could be due to defects in the induction of PCD in response to UV‐B in the root meristem, we evaluated cell death in root tips (Falcone Ferreyra et al, ; Furukawa et al, ; González Besteiro & Ulm, ).…”

“…Our data show that, in the roots, ATM and SOG1 levels are higher in CAF‐1 mutants under controls conditions; therefore, defects in PCD in the mutant roots may be a consequence of altered activation of the DNA damage response. Interestingly, sog1 mutants are defective in damage‐induced PCD, they maintain the cell identities and structure of the stem cell niche immediately after exposure to a genotoxic stress, but meristematic cells fail to undergo cell division after longer exposure times, stopping root growth (Johnson et al, ). SOG1 requires to be phosphorylated by ATM or other kinases to activate DNA damage responses (Yoshiyama et al, ); therefore, in Arabidopsis roots, but not in leaves, a mutation in fas1 or fas2 genes could impair ATM phosphorylation of SOG1 during UV‐B exposure, which in turn may alter activation of the DNA damage response and PCD in particular.…”