E3 ligase SAUL1 serves as a positive regulator of PAMP-triggered immunity and its homeostasis is monitored by immune receptor SOC3.

E3 ligase SAUL1 serves as a positive regulator of PAMP-triggered immunity and its homeostasis is monitored by immune receptor SOC3.
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DOI:
10.1111/nph.14678
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发表时间:
2017-07
期刊:
The New phytologist
影响因子:
--
通讯作者:
Meixuezi Tong;Tanja Kotur;Wanwan Liang;Katja Vogelmann;T. Kleine;D. Leister;Catharina Brieske;Shuhua Yang;Daniel Lüdke;M. Wiermer;Yuelin Zhang;Xin Li;S. Hoth
Meixuezi Tong;Tanja Kotur;Wanwan Liang;Katja Vogelmann;T. Kleine;D. Leister;Catharina Brieske;Shuhua Yang;Daniel Lüdke;M. Wiermer;Yuelin Zhang;Xin Li;S. Hoth
中科院分区:
其他
文献类型:
--
作者:
Meixuezi Tong;Tanja Kotur;Wanwan Liang;Katja Vogelmann;T. Kleine;D. Leister;Catharina Brieske;Shuhua Yang;Daniel Lüdke;M. Wiermer;Yuelin Zhang;Xin Li;S. Hoth

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在植物和动物中,细胞内结合核苷酸的富含亮氨酸的重复蛋白(NLR;或Nod样受体)作为免疫受体识别病原体衍生的分子,并对微生物感染产生有效的免疫反应。植物NLR通常保护其他宿主蛋白的存在或活性,这些蛋白是病原体效应物的直接毒力靶标。这些保护物有时是免疫促进组分,例如促分裂原活化蛋白激酶级联中的那些。植物E3连接酶在免疫调节中起着许多作用,但目前还不清楚它们是否也可以被NLR保护。在这里,我们报告的免疫调节E3连接酶SAUL 1,其稳态监测的Toll白细胞介素1受体(TIR)型NLR(TNL),SOC 3。SOC 3可以与SAUL 1结合,SAUL 1的缺失或过表达触发SOC 3介导的自身免疫。相比之下,SAUL 1与其紧密同源物PUB 43冗余地起作用以促进PAMP触发的免疫(PTI)。总之,E3连接酶SAUL 1作为PTI的正调节剂,其稳态由TNL SOC 3监测。
In both plants and animals, intracellular nucleotide-binding leucine-rich repeat proteins (NLRs; or Nod-like receptors) serve as immune receptors to recognize pathogen-derived molecules and mount effective immune responses against microbial infections. Plant NLRs often guard the presence or activity of other host proteins, which are the direct virulence targets of pathogen effectors. These guardees are sometimes immune-promoting components such as those in a mitogen-activated protein kinase cascade. Plant E3 ligases serve many roles in immune regulation, but it is unclear whether they can also be guarded by NLRs. Here, we report on an immune-regulating E3 ligase SAUL1, whose homeostasis is monitored by a Toll interleukin 1 receptor (TIR)-type NLR (TNL), SOC3. SOC3 can associate with SAUL1, and either loss or overexpression of SAUL1 triggers autoimmunity mediated by SOC3. By contrast, SAUL1 functions redundantly with its close homolog PUB43 to promote PAMP-triggered immunity (PTI). Taken together, the E3 ligase SAUL1 serves as a positive regulator of PTI and its homeostasis is monitored by the TNL SOC3.