Skip to main content
padlock icon - secure page this page is secure

SOG1‐dependent NAC103 modulates the DNA damage response as a transcriptional regulator in Arabidopsis

Buy Article:

$52.00 + tax (Refund Policy)

The plant‐specific transcription factor (TF) NAC103 was previously reported to modulate the unfolded protein response in Arabidopsis under endoplasmic reticulum (ER) stress. Alternatively, we report here that NAC103 is involved in downstream signaling of SOG1, a master regulator for expression of DNA damage response (DDR) genes induced by genotoxic stress. Arabidopsis NAC103 expression was strongly induced by genotoxic stress and nac103 mutants displayed substantial inhibition of DDR gene expression after gamma radiation or radiomimetic zeocin treatment. DDR phenotypes, such as true leaf inhibition, root cell death and root growth inhibition, were also suppressed significantly in the nac103 mutants, but to a lesser extent than in the sog1‐1 mutant. By contrast, overexpression of NAC103 increased DDR gene expression without genotoxic stress and substantially rescued the phenotypic changes in the sog1‐1 mutant after zeocin treatment. The putative promoters of some representative DDR genes, RAD51, PARP1, RPA1E, BRCA1 and At4g22960, were found to partly interact with NAC103. Together with the expected interaction of SOG1 with the promoter of NAC103, our study suggests that NAC103 is a putative SOG1‐dependent transcriptional regulator of plant DDR genes, which are responsible for DDR phenotypes under genotoxic stress.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: Arabidopsis thaliana; DNA damage response; NAC103; SOG1; genotoxic stress; transcriptional regulator

Document Type: Research Article

Publication date: April 1, 2019

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more