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Chlorophylls (Chl) in photosynthetic apparatuses, along with other macromolecules in chloroplasts, are known to undergo degradation during leaf senescence. Several enzymes involved in Chl degradation, by which detoxification of Chl is safely implemented, have been identified. Chl degradation also occurs during embryogenesis and seedling development. Some genes encoding Chl degradation enzymes such as Chl  b  reductase (CBR) function during these developmental stages.  Arabidopsis  mutants lacking CBR (NYC1 and NOL) have been reported to exhibit reduced seed storability, compromised germination, and cotyledon development. In this study, we examined aberrant cotyledon development and found that NYC1 is solely responsible for this phenotype. We inferred that oxidative damage of chloroplast membranes caused the aberrant cotyledon. To test the inference, we attempted to trans-complement  nyc1  mutant with overexpressing VIPP1 protein that is unrelated to Chl degradation but which supports chloroplast membrane integrity. VIPP1 expression actually complemented the aberrant cotyledon of  nyc1 , whereas stay-green phenotype during leaf senescence remained. The swollen chloroplasts observed in unfixed cotyledons of  nyc1 , which are characteristics of chloroplasts receiving envelope membrane damage, were recovered by overexpressing VIPP1. These results suggest that chloroplast membranes are a target for oxidative damage caused by the impairment in Chl degradation. Trans-complementation of  nyc1  with VIPP1 also suggests that VIPP1 is useful for protecting chloroplasts against oxidative stress.

Protection of Chloroplast Membranes by VIPP1 Rescues Aberrant Seedling Development in Arabidopsisnyc1 Mutant