Exportin-4 coordinates nuclear shuttling of TOPLESS family transcription corepressors to regulate plant immunity

编号 040029805

推送时间 20210705

研究领域 森林培育 

年份 2021 

类型 期刊 

语种 英语

标题 Exportin-4 coordinates nuclear shuttling of TOPLESS family transcription corepressors to regulate plant immunity

来源期刊 Molecular Plant

期 第298期

发表时间 20210111

关键词 plant immunity;  Exportin-4;  nuclear transport receptors (NTRs);  stress responses; 

摘要 The regulated nucleocytoplasmic exchange of macromolecules is essential for the eukaryotic cell. However, nuclear transport pathways defined by different nuclear transport receptors (NTRs), including importins and exportins, and their significance in activating distinct stress responses are poorly understood in plants. Here, we exploited a CRISPR/Cas9-based genetic screen to search for modifiers of CONSTITUTIVE EXPRESSION OF PATHOGENESIS-RELATED GENE 5 (cpr5), an Arabidopsis thaliana nucleoporin mutant that activates autoimmune responses that partially mimic effector-triggered immunity (ETI). We identified an NTR gene, Exportin-4 (XPO4), as a genetic interactor of CPR5. The xpo4 cpr5 double mutant activates catastrophic immune responses, which leads to seedling lethality. By leveraging the newly developed proximity-labeling proteomics, we profiled XPO4 substrates and identified TOPLESS (TPL) and TPL-related (TPR) transcription corepressors as XPO4-specific cargo. TPL/TPRs target negative regulators of immunity and are redundantly required for ETI induction. We found that loss-of-XPO4 promotes the nuclear accumulation of TPL/TPRs in the presence of elevated salicylic acid (SA), which contributes to the SA-mediated defense amplification and potentiates immune induction in the cpr5 mutant. We showed that TPL and TPRs are required for the enhanced immune activation observed in xpo4 cpr5 but not for the cpr5 single-mutant phenotype, underscoring the functional interplay between XPO4 and TPL/TPRs and its importance in cpr5-dependent immune induction. We propose that XPO4 coordinates the nuclear accumulation of TPL/TPRs, which plays a role in regulating SA-mediated defense feedback to modulate immune strength downstream of CPR5 during ETI induction.

服务人员 孙小满

服务院士 尹伟伦

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