De-repression of protein phosphatase 5 by the chaperone organizer HOP1 activates plant NLR immunity

分子伴侣组织者HOP1解除对蛋白磷酸酶5的抑制,激活植物NLR免疫。

阅读:1

Abstract

Protein phosphatase 5 (PP5) is a conserved serine/threonine phosphatase regulating growth, stress responses, programmed cell death and immunity across eukaryotes. However, the mechanisms underlying its activation remain poorly understood. Here we demonstrate that the disruption of the plant MEKK1-MKK1/2-MPK4 cascade activates LET7, a plant homologue of PP5, triggering nucleotide-binding leucine-rich repeat (NLR) SUMM2-mediated autoimmunity in Arabidopsis. The binding of LET7 to the co-chaperone protein HOP1 disrupts the autoinhibitory interaction between the tetratricopeptide repeat and phosphatase domains of LET7 in releasing its phosphatase activity. Activated LET7 subsequently dephosphorylates CRCK3, a crucial kinase regulating SUMM2 autoimmunity. Furthermore, HOP1 and LET7 stabilize SUMM2 via their tetratricopeptide repeat domains, highlighting the dual role of the HOP1-LET7 module in dephosphorylating CRCK3 and stabilizing SUMM2 in NLR-mediated immunity. Our studies reveal a conserved mechanism of PP5 activation across plants and animals and elucidate a unique dephosphorylation cascade governing NLR activation.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。