Seed germination or dormancy status is strictly controlled by endogenous phytohormone and exogenous environment signals.Abscisic acid(ABA)is the important phytohormone to suppress seed germination.Ambient high tempera...Seed germination or dormancy status is strictly controlled by endogenous phytohormone and exogenous environment signals.Abscisic acid(ABA)is the important phytohormone to suppress seed germination.Ambient high temperature(HT)also suppressed seed germination,or called as secondary seed dormancy,through upregulating ABI5,the essential component of ABA signal pathway.Previous result shows that appropriate nitric oxide(NO)breaks seed dormancy through triggering S-nitrosoglutathion reductase(GSNOR1)-dependent S-nitrosylation modification of ABI5 protein,subsequently inducing the degradation of ABI5.Here we found that HT induced the degradation of GSNOR1 protein and reduced its activity,thus accumulated more reactive nitrogen species(RNS)to damage seeds viability.Furthermore,HT increased the S-nitrosylation modification of GSNOR1 protein,and triggered the degradation of GSNOR1,therefore stabilizing ABI5 to suppress seed germination.Consistently,the ABI5 protein abundance was lower in the transgenic line overexpressing GSNOR1,but higher in the gsnor mutant after HT stress.Genetic analysis showed that GSNOR1 affected seeds germination through ABI5 under HT.Taken together,our data reveals a new mechanism by which HT triggers the degradation of GSNOR1,and thus stabilizing ABI5 to suppress seed germination,such mechanism provides the possibility to enhance seed germination tolerance to HT through genetic modification of GNSOR1.展开更多
Cross talk between phytohormones, nitric oxide （NO）, and auxin has been implicated in the control of plant growth and development. Two recent reports indicate that NO promoted auxin signaling but inhibited auxin tra...Cross talk between phytohormones, nitric oxide （NO）, and auxin has been implicated in the control of plant growth and development. Two recent reports indicate that NO promoted auxin signaling but inhibited auxin transport probably through S-nitrosylation. However, genetic evidence for the effect of S-nitrosylation on auxin physiology has been lacking. In this study, we used a genetic approach to understand the broader role of S-nitrosylation in auxin physiology in Arabidopsis. We compared auxin signaling and transport in Col-0 and gsnorl-3, a loss-of-function GSNOR1 mutant defective in protein de-nitrosylation. Our results showed that auxin signaling was impaired in the gsnorl-3 mutant as revealed by significantly reduced DR5-GUS/ DR5-GFP accumulation and compromised degradation of AXR3NT-GUS, a useful reporter in interrogating auxin-mediated degradation of Aux/IAA by auxin receptors. In addition, polar auxin transport was compro- mised in gsnorl-3, which was correlated with universally reduced levels of PIN or GFP-PIN proteins in the roots of the mutant in a manner independent of transcription and 26S proteasome degradation. Our results suggest that S-nitrosylation and GSNORl-mediated de-nitrosylation contribute to auxin physiology, and impaired auxin signaling and compromised auxin transport are responsible for the auxin-related morpho- logical phenotypes displayed by the gsnorl-3 mutant.展开更多
基金funded by the National Natural Science Foundation of China(Grants No.31970289).
文摘Seed germination or dormancy status is strictly controlled by endogenous phytohormone and exogenous environment signals.Abscisic acid(ABA)is the important phytohormone to suppress seed germination.Ambient high temperature(HT)also suppressed seed germination,or called as secondary seed dormancy,through upregulating ABI5,the essential component of ABA signal pathway.Previous result shows that appropriate nitric oxide(NO)breaks seed dormancy through triggering S-nitrosoglutathion reductase(GSNOR1)-dependent S-nitrosylation modification of ABI5 protein,subsequently inducing the degradation of ABI5.Here we found that HT induced the degradation of GSNOR1 protein and reduced its activity,thus accumulated more reactive nitrogen species(RNS)to damage seeds viability.Furthermore,HT increased the S-nitrosylation modification of GSNOR1 protein,and triggered the degradation of GSNOR1,therefore stabilizing ABI5 to suppress seed germination.Consistently,the ABI5 protein abundance was lower in the transgenic line overexpressing GSNOR1,but higher in the gsnor mutant after HT stress.Genetic analysis showed that GSNOR1 affected seeds germination through ABI5 under HT.Taken together,our data reveals a new mechanism by which HT triggers the degradation of GSNOR1,and thus stabilizing ABI5 to suppress seed germination,such mechanism provides the possibility to enhance seed germination tolerance to HT through genetic modification of GNSOR1.
基金supported by grants from The National Key Research and Development Program of China(2017YFA0504000)The National Natural Science Foundation of China(31570857,91849203,31800969)~~
文摘Cross talk between phytohormones, nitric oxide （NO）, and auxin has been implicated in the control of plant growth and development. Two recent reports indicate that NO promoted auxin signaling but inhibited auxin transport probably through S-nitrosylation. However, genetic evidence for the effect of S-nitrosylation on auxin physiology has been lacking. In this study, we used a genetic approach to understand the broader role of S-nitrosylation in auxin physiology in Arabidopsis. We compared auxin signaling and transport in Col-0 and gsnorl-3, a loss-of-function GSNOR1 mutant defective in protein de-nitrosylation. Our results showed that auxin signaling was impaired in the gsnorl-3 mutant as revealed by significantly reduced DR5-GUS/ DR5-GFP accumulation and compromised degradation of AXR3NT-GUS, a useful reporter in interrogating auxin-mediated degradation of Aux/IAA by auxin receptors. In addition, polar auxin transport was compro- mised in gsnorl-3, which was correlated with universally reduced levels of PIN or GFP-PIN proteins in the roots of the mutant in a manner independent of transcription and 26S proteasome degradation. Our results suggest that S-nitrosylation and GSNORl-mediated de-nitrosylation contribute to auxin physiology, and impaired auxin signaling and compromised auxin transport are responsible for the auxin-related morpho- logical phenotypes displayed by the gsnorl-3 mutant.
