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Although research has determined that reactive oxygen species (ROS) function as signaling molecules in plant development, the molecular mechanism by which ROS regulate plant growth is not well known. An   ab  a   o  verly sensitive mutant,  abo8-1 , which is defective in a pentatricopeptide repeat (PPR) protein responsible for the splicing of  NAD4  intron 3 in mitochondrial complex I, accumulates more ROS in root tips than the wild type, and the ROS accumulation is further enhanced by ABA treatment. The  ABO8  mutation reduces root meristem activity, which can be enhanced by ABA treatment and reversibly recovered by addition of certain concentrations of the reducing agent GSH. As indicated by low  ProDR5:GUS  expression, auxin accumulation/signaling was reduced in  abo8-1 . We also found that ABA inhibits the expression of  PLETHORA1  ( PLT1 ) and  PLT2 , and that root growth is more sensitive to ABA in the  plt1  and  plt2  mutants than in the wild type. The expression of  PLT1  and  PLT2  is significantly reduced in the  abo8-1  mutant. Overexpression of PLT2 in an inducible system can largely rescue root apical meristem (RAM)-defective phenotype of  abo8-1  with and without ABA treatment. These results suggest that ABA-promoted ROS in the mitochondria of root tips are important retrograde signals that regulate root meristem activity by controlling auxin accumulation/signaling and  PLT  expression in  Arabidopsis .

ABA-Mediated ROS in Mitochondria Regulate Root Meristem Activity by Controlling PLETHORA Expression in Arabidopsis