Programmed cell death(PCD)is essential for both plant development and stress responses including immunity.However,how plants control PCD is not well-understood.The shikimate pathway is one of the most important metabo...Programmed cell death(PCD)is essential for both plant development and stress responses including immunity.However,how plants control PCD is not well-understood.The shikimate pathway is one of the most important metabolic pathways in plants,but its relationship to PCD is unknown.Here,we show that the shikimate pathway promotes PCD in Arabidopsis.We identify a photoperiod-dependent lesion-mimic mutant named Lesion in short-day(lis),which forms spontaneous lesions in short-day conditions.Mapbased cloning and whole-genome resequencing reveal that LIS encodes MEE32,a bifunctional enzyme in the shikimate pathway.Metabolic analysis shows that the level of shikimate is dramatically increased in lis.Through genetic screenings,three suppressors of lis(slis)are identified and the causal genes are cloned.SLISes encode proteins upstream of MEE32 in the shikimate pathway.Furthermore,exogenous shikimate treatment causes PCD.Our study uncovers a link between the shikimate pathway and PCD,and suggests that the accumulation of shikimate is an alternative explanation for the action of glyphosate,the most successful herbicide.展开更多
It is well known that plants activate defense responses at the cost of growth.However,the underlying molecular mechanisms are not well understood.The phytohormones salicylic acid(SA)and gibberellin(GA)promote defense ...It is well known that plants activate defense responses at the cost of growth.However,the underlying molecular mechanisms are not well understood.The phytohormones salicylic acid(SA)and gibberellin(GA)promote defense response and growth,respectively.Here we show that SA inhibits GA signaling to repress plant growth.We found that the SA receptor NPR1 interacts with the GA receptor GID1.Further biochemical studies revealed that NPR1 functions as an adaptor of ubiquitin E3 ligase to promote the polyubiquitination and degradation of GID1,which enhances the stability of DELLA proteins,the negative regulators of GA signaling.Genetic analysis suggested that NPR1,GID1,and DELLA proteins are all required for the SA-mediated growth inhibition.Collectively,our study not only uncovers a novel regulatory mechanism of growth-defense trade-off but also reveals the interaction of hormone receptors as a new mode of hormonal crosstalk.展开更多
基金supported by grants from the National Natural Science Foundation of China(31771355,31970311)Thousand Talents Plan of China-Young ProfessionalsHuazhong Agricultural University Scientific&Technological Self-innovation Foundation(2014RC004)。
文摘Programmed cell death(PCD)is essential for both plant development and stress responses including immunity.However,how plants control PCD is not well-understood.The shikimate pathway is one of the most important metabolic pathways in plants,but its relationship to PCD is unknown.Here,we show that the shikimate pathway promotes PCD in Arabidopsis.We identify a photoperiod-dependent lesion-mimic mutant named Lesion in short-day(lis),which forms spontaneous lesions in short-day conditions.Mapbased cloning and whole-genome resequencing reveal that LIS encodes MEE32,a bifunctional enzyme in the shikimate pathway.Metabolic analysis shows that the level of shikimate is dramatically increased in lis.Through genetic screenings,three suppressors of lis(slis)are identified and the causal genes are cloned.SLISes encode proteins upstream of MEE32 in the shikimate pathway.Furthermore,exogenous shikimate treatment causes PCD.Our study uncovers a link between the shikimate pathway and PCD,and suggests that the accumulation of shikimate is an alternative explanation for the action of glyphosate,the most successful herbicide.
文摘It is well known that plants activate defense responses at the cost of growth.However,the underlying molecular mechanisms are not well understood.The phytohormones salicylic acid(SA)and gibberellin(GA)promote defense response and growth,respectively.Here we show that SA inhibits GA signaling to repress plant growth.We found that the SA receptor NPR1 interacts with the GA receptor GID1.Further biochemical studies revealed that NPR1 functions as an adaptor of ubiquitin E3 ligase to promote the polyubiquitination and degradation of GID1,which enhances the stability of DELLA proteins,the negative regulators of GA signaling.Genetic analysis suggested that NPR1,GID1,and DELLA proteins are all required for the SA-mediated growth inhibition.Collectively,our study not only uncovers a novel regulatory mechanism of growth-defense trade-off but also reveals the interaction of hormone receptors as a new mode of hormonal crosstalk.
