Limitation of nocturnal import of ATP into Arabidopsis chloroplasts leads to photooxidative damage.

摘要: Summary When grown in short day conditions and at low light, leaves of Arabidopsis plants with mutations the genes encoding two plastidial ATP/ADP transporters (so-called null mutants) spontaneously develop necrotic lesions. Under these conditions, mutants also display light-induced accumulation H2O2 constitutive expression for copper/zinc superoxide dismutase 2 ascorbate peroxidase 1. In light phase, accumulate high levels phototoxic protoporphyrin IX but have only slightly reduced Mg protoporphyrin IX. The physiological changes are associated magnesium–chelatase activity. Since any three subunits is similar wild type mutants, decreased enzyme activity probably due to post-translational modification which might be limited availability ATP plastids during night. Surprisingly, formation lesions was absent when were either long days intensity or intensity. We ascribe lack lesion phenotype increased nocturnal supply glycolytic degradation starch may lead additional substrate-level phosphorylation stroma. Thus, import into chloroplasts represents a crucial, previously unknown process that required controlled chlorophyll biosynthesis preventing photooxidative damage.