Upregulated expression of RESPIRATORY BURST OXIDASE HOMOLOG D underlies lesion-mimic phenotype in dark-treated Arabidopsis pheide a oxygenase mutant leaves.

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CONCLUSION: Upregulated expression of RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) encoding a plasma membrane NADPH oxidase is responsible for the lesion-mimic phenotype in detached Arabidopsis leaves with mutation of PHEIDE a OXYGENASE during extended darkness. Chlorophyll degradation is an indispensable process in leaf senescence, either age-dependent or dark-induced. Besides higher chlorophyll retention, a lesion-mimic phenotype (abbreviated as LMP afterwards) was exhibited in Arabidopsis leaves with mutation of PHEIDE a OXYGENASE (PaO) involved in chlorophyll degradation during dark incubation, but the associated mechanism remains elusive. We found that dark-treated pao leaves showed higher membrane damage and H2O2 accumulation, while scavenging H2O2 by its chemical scavenger diminished LMP. RBOHD which encodes NADPH oxidase was strikingly up-regulated in pao leaves during dark treatment. Chemical inhibition of NADPH oxidase or mutation of RBOHD in pao leaves suppressed LMP. Thus, our study suggests that up-regulated RBOHD transcription is responsible for the formation of LMP in dark-treated pao leaves and there may be a retrograde signaling pathway mediating upregulation of RBOHD which remains to be elucidated.