Wu Zhongshou, Huang Shuai, Zhang Xiaobo, Wu Di, Xia Shitou, Li Xin
Michael Smith Laboratories, University of British Columbia, Vancouver, Canada.
Department of Botany, University of British Columbia, Vancouver, Canada.
Elife. 2017 Mar 31;6:e23684. doi: 10.7554/eLife.23684.
Plant immunity is tightly regulated to ensure proper defense against surrounding microbial pathogens without triggering autoimmunity, which negatively impacts plant growth and development. Immune receptor levels are intricately controlled by RNA processing and post-translational modification events, such as ubiquitination. It remains unknown whether, and if yes, how, plant immune receptor homeostasis is regulated at the translational level. From a , () forward genetic screen, we identified MUSE11/EXA1, which negatively regulates nucleotide-binding leucine-rich repeat (NLR) receptor mediated defence. EXA1 contains an evolutionarily conserved glycine-tyrosine-phenylalanine (GYF) domain that binds proline-rich sequences. Genetic and biochemical analysis revealed that loss of leads to heightened NLR accumulation and enhanced resistance against virulent pathogens. EXA1 also associates with eIF4E initiation factors and the ribosome complex, likely contributing to the proper translation of target proteins. In summary, our study reveals a previously unknown mechanism of regulating NLR homeostasis through translational repression by a GYF protein.
植物免疫受到严格调控,以确保在不引发自身免疫的情况下对周围微生物病原体进行适当防御,自身免疫会对植物生长发育产生负面影响。免疫受体水平受到RNA加工和翻译后修饰事件(如泛素化)的复杂控制。目前尚不清楚植物免疫受体稳态是否以及如何在翻译水平上受到调控。通过正向遗传筛选,我们鉴定出了MUSE11/EXA1,它对核苷酸结合富含亮氨酸重复序列(NLR)受体介导的防御起负调控作用。EXA1包含一个与富含脯氨酸序列结合的进化保守甘氨酸-酪氨酸-苯丙氨酸(GYF)结构域。遗传和生化分析表明,EXA1缺失会导致NLR积累增加,并增强对致病病原体的抗性。EXA1还与eIF4E起始因子和核糖体复合物相关联,可能有助于靶蛋白的正确翻译。总之,我们的研究揭示了一种以前未知的通过GYF蛋白进行翻译抑制来调控NLR稳态的机制。