Drought stress and abscisic acid(ABA)have been known to play a critical role in modulating sugar accumulation in fruit,and yet,the underlying molecular mechanisms remain elusive.In this study,we have demonstrated that...Drought stress and abscisic acid(ABA)have been known to play a critical role in modulating sugar accumulation in fruit,and yet,the underlying molecular mechanisms remain elusive.In this study,we have demonstrated that drought-mimicking film mulching increased sucrose levels in Satsuma mandarin(Citrus unshiu)fruit,coinciding with upregulation of CuSPS4,which encodes the sucrose phosphate synthase(SPS),in the transcriptome profiling.CuSPS4 was further shown to be drought-and ABA-inducible and functionally essential for sucrose synthesis.Mechanistically,two transcription factors,CuWRKY41 and CuWRKY23,directly bound to and activated the CuSPS4 promoter via the W-box element,with CuWRKY41 additionally regulating CuWRKY23 expression.Consistently,both Cu WRKY41 and Cu WRKY23 positively regulated sucrose synthesis by upregulating Cu SPS4.Meanwhile,the ubstrateinteracting subunit(Cu Sn RK1β1)and catalytic subunit(Cu Sn RK1α)of SUCROSE NON-FERMENTING RELATED KINASE 1(Sn RK1)interacted with Cu WRKY41,triggering Cu Sn RK1α-mediated phosphorylation and subsequent degradation of Cu WRKY41,thereby suppressing its activation.However,ABA promoted cytoplasmic translocation of Cu Sn RK1αand Cu Sn RK1β1 and reduced nuclear interaction with Cu WRKY41,leading to its phosphorylation alleviation and protein stabilization,concurrent with enhanced transcription activation of Cu WRKY23 and Cu SPS4.Taken together,these findings reveal a sophisticated regulatory mechanism whereby drought promotes sucrose accumulation by suppressing Cu Sn RK1α-mediated phosphorylation and degradation of Cu WRKY41,enabling its transcriptional activation of Cu SPS4 directly or via Cu WRKY23.Our study provides significant insights into the molecular basis of drought-induced sucrose accumulation and presents valuable regulatory components that could be targeted for fruit quality improvement.展开更多
基金supported by the National Natural Science Foundation of China(32330095)the Hubei Hongshan Laboratory project(2021hszd009)。
文摘Drought stress and abscisic acid(ABA)have been known to play a critical role in modulating sugar accumulation in fruit,and yet,the underlying molecular mechanisms remain elusive.In this study,we have demonstrated that drought-mimicking film mulching increased sucrose levels in Satsuma mandarin(Citrus unshiu)fruit,coinciding with upregulation of CuSPS4,which encodes the sucrose phosphate synthase(SPS),in the transcriptome profiling.CuSPS4 was further shown to be drought-and ABA-inducible and functionally essential for sucrose synthesis.Mechanistically,two transcription factors,CuWRKY41 and CuWRKY23,directly bound to and activated the CuSPS4 promoter via the W-box element,with CuWRKY41 additionally regulating CuWRKY23 expression.Consistently,both Cu WRKY41 and Cu WRKY23 positively regulated sucrose synthesis by upregulating Cu SPS4.Meanwhile,the ubstrateinteracting subunit(Cu Sn RK1β1)and catalytic subunit(Cu Sn RK1α)of SUCROSE NON-FERMENTING RELATED KINASE 1(Sn RK1)interacted with Cu WRKY41,triggering Cu Sn RK1α-mediated phosphorylation and subsequent degradation of Cu WRKY41,thereby suppressing its activation.However,ABA promoted cytoplasmic translocation of Cu Sn RK1αand Cu Sn RK1β1 and reduced nuclear interaction with Cu WRKY41,leading to its phosphorylation alleviation and protein stabilization,concurrent with enhanced transcription activation of Cu WRKY23 and Cu SPS4.Taken together,these findings reveal a sophisticated regulatory mechanism whereby drought promotes sucrose accumulation by suppressing Cu Sn RK1α-mediated phosphorylation and degradation of Cu WRKY41,enabling its transcriptional activation of Cu SPS4 directly or via Cu WRKY23.Our study provides significant insights into the molecular basis of drought-induced sucrose accumulation and presents valuable regulatory components that could be targeted for fruit quality improvement.
