ABA signaling prevents phosphodegradation of the SR45 splicing factor to alleviate inhibition of early seedling development in Arabidopsis
作者机构:Instituto Gulbenkian de Ciencia2780-156 OeirasPortugal Sainsbury LaboratoryUniversity of CambridgeCambridge B21LRUK
出 版 物:《Plant Communications》 (植物通讯(英文))
年 卷 期:2023年第4卷第2期
页 面:272-285页
核心收录:
学科分类:0710[理学-生物学] 071001[理学-植物学] 07[理学]
基 金:This work was funded by the Fundac¸ao para a Ciencia e a Tecnologia(FCT)through grant PTDC/ASP-PLA/2550/2021 and a PhD fellowship PD/BD/128401/2017 awarded to R.A.-M.Funding from the research unit GREEN-it"Bioresources for Sustainability"(UIDB/04551/2020)is also acknowledged A.M.J.and J.R.were funded by the Gatsby Charitable Foundation and BBSRC(BB/P018572/1)
主 题:abscisic acid alternative splicing Arabidopsis thaliana protein phosphorylation SR proteins
摘 要:Serine/arginine-rich(SR)proteins are conserved splicing regulators that play important roles in plant stress responses,namely those mediated by the abscisic acid(ABA)*** Arabidopsis thaliana SR-like protein SR45 is a described negative regulator of the ABA pathway during early seedling *** the inhibition of growth by ABA signaling is counteracted to maintain plant development under stress conditions remains largely ***,we show that SR45 overexpression reduces Arabidopsis sensitivity to ABA during early seedling *** and confocal microscopy analyses of transgenic plants expressing fluorescently tagged SR45 revealed that exposure to ABA dephosphorylates the protein at multiple amino acid residues and leads to its accumulation,due to SR45 stabilization via reduced ubiquitination and proteasomal *** phosphomutant and phosphomimetic transgenic Arabidopsis lines,we demonstrate the functional relevance of ABA-mediated dephosphorylation of a single SR45 residue,T264,in antagonizing SR45 ubiquitination and degradation to promote its function as a repressor of seedling ABA *** results reveal a mechanism that negatively autoregulates ABA signaling and allows early plant growth under stress via posttranslational control of the SR45 splicing factor.