| Categories genes  | Tags leaf  leaf senescence  senescence  mitochondria  map-based cloning  oxidative  redox homeostasis 
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    • In a further feeding assay with exogenous glutathione (GSH), a non-enzymatic antioxidant that consumes H2O2, the H2O2 accumulation and leaf senescence phenotypes of hpa1 were obviously compensated
    • Taken together, our findings suggest that the accumulation of H2O2 in hpa1 may be mediated by an altered folate status and redox homeostasis, subsequently triggering leaf senescence
    • Proteomics and enzyme activity analyses further revealed that mitochondria oxidative phosphorylation complex I and complex V were differentially expressed in hpa1, which was consistent with the H2O2 accumulation in hpa1
    • Map-based cloning revealed that HPA1 encodes a tetrahydrofolate deformylase, and its deficiency led to the accumulation of tetrahydrofolate, 5-formyl tetrahydrofolate and 10-formyl tetrahydrofolate, in contrast, a decrease in 5,10-methenyl-tetrahydrofolate
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