Selective regulation of the chitin-induced defense response by the Arabidopsis receptor-like cytoplasmic kinase PBL27

Selective regulation of the chitin-induced defense response by the Arabidopsis receptor-like cytoplasmic kinase PBL27
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DOI:
10.1111/tpj.12535
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发表时间:
2014-07-01
期刊:
影响因子:
7.2
通讯作者:
Shibuya, Naoto
Shibuya, Naoto
中科院分区:
生物学1区
文献类型:
--
作者:
Shinya, Tomonori;Yamaguchi, Koji;Shibuya, Naoto

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微生物相关分子模式(MAMPs)的识别在寄主植物中启动模式触发免疫。模式识别受体(PRRs)和受体样胞浆激活酶(RLCK)是感知和转导这些分子模式所必需的主要成分。然而,PRRs对RLCK的调控及其特异性仍然不清楚。在这项研究中,我们证明了PBL27,一个与OsRLCK185同源的拟南芥基因,是几丁质受体CERK1的直接下游成分,参与了几丁质诱导的拟南芥免疫的调节。PBL27基因敲除导致了几种甲壳素诱导的防御反应的抑制,包括MPK3/6的激活和痂蛋白的沉积,以及对真菌和细菌感染的抗病能力。另一方面,PBL27对flg22信号的贡献似乎非常有限,这表明PBL27选择性地调节特定PRR复合体下游的防御信号。体外磷酸化实验表明,与BIK1相比,CERK1优先磷酸化PBL27,而BAK1对PBL27的磷酸化程度比BIK1低。因此,信号受体样激酶CERK1和BAK1的底物特异性可能决定了下游RLCKs的偏好。
Recognition of microbe-associated molecular patterns (MAMPs) initiates pattern-triggered immunity in host plants. Pattern recognition receptors (PRRs) and receptor-like cytoplasmic kinases (RLCKs) are the major components required for sensing and transduction of these molecular patterns. However, the regulation of RLCKs by PRRs and their specificity remain obscure. In this study we show that PBL27, an Arabidopsis ortholog of OsRLCK185, is an immediate downstream component of the chitin receptor CERK1 and contributes to the regulation of chitin-induced immunity in Arabidopsis. Knockout of PBL27 resulted in the suppression of several chitin-induced defense responses, including the activation of MPK3/6 and callose deposition as well as in disease resistance against fungal and bacterial infections. On the other hand, the contribution of PBL27 to flg22 signaling appears to be very limited, suggesting that PBL27 selectively regulates defense signaling downstream of specific PRR complexes. In vitro phosphorylation experiments showed that CERK1 preferentially phosphorylated PBL27 in comparison to BIK1, whereas phosphorylation of PBL27 by BAK1 was very low compared with that of BIK1. Thus, the substrate specificity of the signaling receptor-like kinases, CERK1 and BAK1, may determine the preference of downstream RLCKs.