Senescence-induced NAC(senNAC)TFs play a crucial role in senescence during the final stage of leaf development.In this study,we identified a rice senNAC,ONAC016,which functions as a positive regulator of leaf senescen...Senescence-induced NAC(senNAC)TFs play a crucial role in senescence during the final stage of leaf development.In this study,we identified a rice senNAC,ONAC016,which functions as a positive regulator of leaf senescence.The expression of ONAC016 increased rapidly in rice leaves during the progression of dark-induced and natural senescence.The onac016-1 knockout mutant showed a delayed leaf yellowing phenotype,whereas the overexpression of ONAC016 accelerated leaf senescence.Notably,ONAC016 expression was upregulated by abscisic acid(ABA),and thus detached leaves of the onac016-1 mutant remained green much longer under ABA treatment.Quantitative RT-PCR analysis showed that ONAC016 upregulates the genes associated with chlorophyll degradation,senescence,and ABA signaling.Yeast one-hybrid and dual-luciferase assays revealed that ONAC016 binds directly to the promoter regions of OsNAP,a key gene involved in chlorophyll degradation and ABA-induced senescence.Taken together,these results suggest that ONAC016 plays an important role in promoting leaf senescence through the ABA signaling pathway involving OsNAP.展开更多
The small ubiquitin-related modifier （SUMO） modification plays an important role in the regulation of abscisic acid （ABA） signaling, but the function of the SUMO protease, in ABA signaling, remains largely unknown...The small ubiquitin-related modifier （SUMO） modification plays an important role in the regulation of abscisic acid （ABA） signaling, but the function of the SUMO protease, in ABA signaling, remains largely unknown. Here, we show that the SUMO protease, ASPI positively regulates ABA signaling. Mutations in ASPI resulted in an ABA-insensitive phenotype, during early seedling develop- ment. Wild-type ASP1 successfully rescued, whereas an ASPI mutant （C577S）, defective in SUMO protease activity, failed to rescue, the ABA-insensitive phenotype of asp1-1. Expression of ABI5 and MYB3o target genes was attenuated in asp^-I and our genetic analyses revealed that ASP1 may function upstream of ABI5 and MYB3o.展开更多
基金supported by the National Research Foundation of Korea(NRF)grant funded by the Korea government(MSIT)(2022R1A2C1091553 to Nam-Chon Paek and 2022R1F1A1075022 to Kiyoon Kang)。
文摘Senescence-induced NAC(senNAC)TFs play a crucial role in senescence during the final stage of leaf development.In this study,we identified a rice senNAC,ONAC016,which functions as a positive regulator of leaf senescence.The expression of ONAC016 increased rapidly in rice leaves during the progression of dark-induced and natural senescence.The onac016-1 knockout mutant showed a delayed leaf yellowing phenotype,whereas the overexpression of ONAC016 accelerated leaf senescence.Notably,ONAC016 expression was upregulated by abscisic acid(ABA),and thus detached leaves of the onac016-1 mutant remained green much longer under ABA treatment.Quantitative RT-PCR analysis showed that ONAC016 upregulates the genes associated with chlorophyll degradation,senescence,and ABA signaling.Yeast one-hybrid and dual-luciferase assays revealed that ONAC016 binds directly to the promoter regions of OsNAP,a key gene involved in chlorophyll degradation and ABA-induced senescence.Taken together,these results suggest that ONAC016 plays an important role in promoting leaf senescence through the ABA signaling pathway involving OsNAP.
基金supported by grants from the National Natural Science Foundation of China(31670186)the Chinese Academy of Sciences(XDA08010105)
文摘The small ubiquitin-related modifier （SUMO） modification plays an important role in the regulation of abscisic acid （ABA） signaling, but the function of the SUMO protease, in ABA signaling, remains largely unknown. Here, we show that the SUMO protease, ASPI positively regulates ABA signaling. Mutations in ASPI resulted in an ABA-insensitive phenotype, during early seedling develop- ment. Wild-type ASP1 successfully rescued, whereas an ASPI mutant （C577S）, defective in SUMO protease activity, failed to rescue, the ABA-insensitive phenotype of asp1-1. Expression of ABI5 and MYB3o target genes was attenuated in asp^-I and our genetic analyses revealed that ASP1 may function upstream of ABI5 and MYB3o.
