Dehydrating stresses trigger the accumulation of abscisic acid(ABA),a key plant stress-signaling hormone that activates Snf1-Related Kinases(SnRK2s)to mount adaptive responses.However,the regulatory circuits that term...Dehydrating stresses trigger the accumulation of abscisic acid(ABA),a key plant stress-signaling hormone that activates Snf1-Related Kinases(SnRK2s)to mount adaptive responses.However,the regulatory circuits that terminate the SnRK2s signal relay after acclimation or post-stress conditions remain to be defined.Here,we show that the desensitization of the ABA signal is achieved by the regulation of OST1(SnRK2.6)protein stability via the E3-ubiquitin ligase HOS15.Upon ABA signal,HOS15-induced degradation of OST1 is inhibited and stabilized OST1 promotes the stress response.When the ABA signal terminates,protein phosphatases ABI1/2 promote rapid degradation of OST1 via HOS15.Notably,we found that even in the presence of ABA,OST1 levels are also depleted within hours of ABA signal onset.The unexpected dynamics of OST1 abundance are then resolved by systematic mathematical modeling,demonstrating a desensitizing feedback loop by which OST1-induced upregulation of ABI1/2 leads to the degradation of OST1.This model illustrates the complex rheostat dynamics underlying the ABA-induced stress response and desensitization.展开更多
Flowering is the primary stage of the plant developmental transition and is tightly regulated by environmental factors such as light and temperature.However,the mechanisms by which temperature signals are integrated i...Flowering is the primary stage of the plant developmental transition and is tightly regulated by environmental factors such as light and temperature.However,the mechanisms by which temperature signals are integrated into the photoperiodic flowering pathway are still poorly understood.Here,we demonstrate that HOS15,which is known as a GI transcriptional repressor in the photoperiodic flowering pathway,controls flowering time in response to low ambient temperature.At 16℃,the hos15 mutant exhibits an early flowering phenotype,and HOS15 acts upstream of photoperiodic flowering genes(GI,CO,and FT).GI protein abundance is increased in the hos15 mutant and is insensitive to the proteasome inhibitor MG132.Furthermore,the hos15 mutant has a defect in low ambient temperature-mediated GI degradation,and HOS15 interacts with COP1,an E3 ubiquitin ligase for GI degradation.Phenotypic analyses of the hos15 cop1 double mutant revealed that repression of flowering by HOS15 is dependent on COP1 at 16℃.However,the HOS15-COP1 interaction was attenuated at 16℃,and GI protein abundance was additively increased in the hos15 cop1 double mutant,indicating that HOS15 acts independently of COP1 in GI turnover at low ambient temperature.This study proposes that HOS15 controls GI abundance through multiple modes as an E3 ubiquitin ligase and transcriptional repressor to coordinate appropriate flowering time in response to ambient environmental conditions such as temperature and day length.展开更多
文摘Dehydrating stresses trigger the accumulation of abscisic acid(ABA),a key plant stress-signaling hormone that activates Snf1-Related Kinases(SnRK2s)to mount adaptive responses.However,the regulatory circuits that terminate the SnRK2s signal relay after acclimation or post-stress conditions remain to be defined.Here,we show that the desensitization of the ABA signal is achieved by the regulation of OST1(SnRK2.6)protein stability via the E3-ubiquitin ligase HOS15.Upon ABA signal,HOS15-induced degradation of OST1 is inhibited and stabilized OST1 promotes the stress response.When the ABA signal terminates,protein phosphatases ABI1/2 promote rapid degradation of OST1 via HOS15.Notably,we found that even in the presence of ABA,OST1 levels are also depleted within hours of ABA signal onset.The unexpected dynamics of OST1 abundance are then resolved by systematic mathematical modeling,demonstrating a desensitizing feedback loop by which OST1-induced upregulation of ABI1/2 leads to the degradation of OST1.This model illustrates the complex rheostat dynamics underlying the ABA-induced stress response and desensitization.
基金This research was supported by National Research Foundation of Korea(NRF)grants funded by the Korean Government(MSIT-2022R1A5A1031361 and MSIT-2020R1A2C3014814 to W.-Y.K.)the Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education(NRF-2021R1I1A1A01059532 to G.A.and NRF-2019R1I1A1A01041422 to H.J.P.)。
文摘Flowering is the primary stage of the plant developmental transition and is tightly regulated by environmental factors such as light and temperature.However,the mechanisms by which temperature signals are integrated into the photoperiodic flowering pathway are still poorly understood.Here,we demonstrate that HOS15,which is known as a GI transcriptional repressor in the photoperiodic flowering pathway,controls flowering time in response to low ambient temperature.At 16℃,the hos15 mutant exhibits an early flowering phenotype,and HOS15 acts upstream of photoperiodic flowering genes(GI,CO,and FT).GI protein abundance is increased in the hos15 mutant and is insensitive to the proteasome inhibitor MG132.Furthermore,the hos15 mutant has a defect in low ambient temperature-mediated GI degradation,and HOS15 interacts with COP1,an E3 ubiquitin ligase for GI degradation.Phenotypic analyses of the hos15 cop1 double mutant revealed that repression of flowering by HOS15 is dependent on COP1 at 16℃.However,the HOS15-COP1 interaction was attenuated at 16℃,and GI protein abundance was additively increased in the hos15 cop1 double mutant,indicating that HOS15 acts independently of COP1 in GI turnover at low ambient temperature.This study proposes that HOS15 controls GI abundance through multiple modes as an E3 ubiquitin ligase and transcriptional repressor to coordinate appropriate flowering time in response to ambient environmental conditions such as temperature and day length.
