EIN3 and ORE1 Accelerate Degreening during Ethylene-Mediated Leaf Senescence by Directly Activating Chlorophyll Catabolic Genes in
Yellowing, caused by chlorophyll degradation, is the most obvious symptom of senescent leaves. Chlorophyll degradation can be triggered by a broad range of endogenous and environmental cues, and ethylene is one of the major inducers. Yet, the molecular regulation of chlorophyll degradation remains largely unknown. Here, we report a feed-forward regulation of ethylene-mediated chlorophyll degradation that involves ETHYLENE INSENSITIVE3 (EIN3), ORE1/NAC2, and major chlorophyll catabolic genes. EIN3, a master positive regulator of ethylene signaling, could directly promote chlorophyll degradation by physically binding to the promoters of three major chlorophyll catabolic genes to activate their expressions. Meanwhile, ORE1, a direct target of EIN3, also activates the expression of the similar set of chlorophyll catabolic genes directly. Moreover, ORE1 activates the expression of a major ethylene biosynthesis gene ACS2 during senescence, and subsequently activates a positive feedback to ethylene synthesis. Our work reveals a feed-forward loop that promotes ethylene-mediated chlorophyll degradation during leaf senescence, advancing our understanding on the molecular mechanism of leaf yellowing.
Vyšlo v časopise:
EIN3 and ORE1 Accelerate Degreening during Ethylene-Mediated Leaf Senescence by Directly Activating Chlorophyll Catabolic Genes in. PLoS Genet 11(7): e32767. doi:10.1371/journal.pgen.1005399
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.pgen.1005399
Souhrn
Yellowing, caused by chlorophyll degradation, is the most obvious symptom of senescent leaves. Chlorophyll degradation can be triggered by a broad range of endogenous and environmental cues, and ethylene is one of the major inducers. Yet, the molecular regulation of chlorophyll degradation remains largely unknown. Here, we report a feed-forward regulation of ethylene-mediated chlorophyll degradation that involves ETHYLENE INSENSITIVE3 (EIN3), ORE1/NAC2, and major chlorophyll catabolic genes. EIN3, a master positive regulator of ethylene signaling, could directly promote chlorophyll degradation by physically binding to the promoters of three major chlorophyll catabolic genes to activate their expressions. Meanwhile, ORE1, a direct target of EIN3, also activates the expression of the similar set of chlorophyll catabolic genes directly. Moreover, ORE1 activates the expression of a major ethylene biosynthesis gene ACS2 during senescence, and subsequently activates a positive feedback to ethylene synthesis. Our work reveals a feed-forward loop that promotes ethylene-mediated chlorophyll degradation during leaf senescence, advancing our understanding on the molecular mechanism of leaf yellowing.
Zdroje
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Genetika Reprodukčná medicínaČlánok vyšiel v časopise
PLOS Genetics
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