A shared DNA-damage-response pathway for induction of stem-cell death by UVB and by gamma irradiation

DNA Repair (Amst). 2010 Sep 4;9(9):940-8. doi: 10.1016/j.dnarep.2010.06.006. Epub 2010 Jul 15.

Abstract

Both UVB radiation and DNA-breaking agents were previously reported to kill Arabidopsis stem cells. We demonstrate that death induced by UVB or by ionizing radiation (IR) requires Suppressor of Gamma Response 1 (SOG1), a transcription factor already found to govern many responses to these agents in Arabidopsis. DNA-damage responses (DDRs) triggered primarily by replication-blocking photoadducts or double-strand-breaks thus converge to a shared programmed-cell-death (PCD) pathway. Both UVB- and IR-induced PCD also require functional DDR protein kinases. Employment of atr atm mutants (uniquely available in Arabidopsis) shows that either ATR (which recognizes ssDNA) or ATM (which recognizes DSBs) suffices for PCD induction by either agent. Thus, DNA damage made by UVB or by IR engenders both ATM-activating and ATR-activating structures. The elevated PCD in UVB-irradiated atr and atm mutants suggests that in wt plants ATR and/or ATM may activate both pathways that avert PCD and those that elicit it. The similar PCD levels induced by roughly 30,000 unrepaired photoadducts vs. 20 IR-induced DSBs indicate that DDR damage-tolerance activities in this model stem-cell niche are remarkably efficient.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins
  • Base Sequence
  • Cell Cycle Proteins / metabolism
  • Cell Death / radiation effects*
  • DNA Damage*
  • DNA Primers
  • DNA-Binding Proteins / metabolism
  • Gamma Rays*
  • Humans
  • Polymerase Chain Reaction
  • Protein-Serine-Threonine Kinases / metabolism
  • Stem Cells / radiation effects*
  • Tumor Suppressor Proteins / metabolism
  • Ultraviolet Rays*

Substances

  • Cell Cycle Proteins
  • DNA Primers
  • DNA-Binding Proteins
  • Tumor Suppressor Proteins
  • ATM protein, human
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein-Serine-Threonine Kinases