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Co-regulation of indole glucosinolates and camalexin biosynthesis by CPK5/CPK6 and MPK3/MPK6 signaling pathways.
Journal of Integrative Plant Biology ( IF 9.3 ) Pub Date : 2020-05-25 , DOI: 10.1111/jipb.12973
Liuyi Yang 1 , Yan Zhang 1 , Rongxia Guan 2 , Sen Li 1 , Xuwen Xu 1 , Shuqun Zhang 3 , Juan Xu 1
Affiliation  

Secondary plant metabolites, represented by indole glucosinolates (IGS) and camalexin, play important roles in Arabidopsis immunity. Previously, we demonstrated the importance of MPK3 and MPK6, two closely related MAPKs, in regulating Botrytis cinerea (Bc)‐induced IGS and camalexin biosynthesis. Here we report that CPK5 and CPK6, two redundant calcium‐dependent protein kinases (CPKs), are also involved in regulating the biosynthesis of these secondary metabolites. The loss‐of‐function of both CPK5 and CPK6 compromises plant resistance to Bc. Expression profiling of CPK5‐VK transgenic plants, in which a truncated constitutively active CPK5 is driven by a steroid‐inducible promoter, revealed that biosynthetic genes of both IGS and camalexin pathways are coordinately upregulated after the induction of CPK5‐VK, leading to high‐level accumulation of camalexin and 4‐methoxyindole‐3‐yl‐methylglucosinolate (4MI3G). Induction of camalexin and 4MI3G, as well as the genes in their biosynthesis pathways, is greatly compromised in cpk5 cpk6 mutant in response to Bc. In a conditional cpk5 cpk6 mpk3 mpk6 quadruple mutant, Bc resistance and induction of IGS and camalexin are further reduced in comparison to either cpk5 cpk6 or conditional mpk3 mpk6 double mutant, suggesting that both CPK5/CPK6 and MPK3/MPK6 signaling pathways contribute to promote the biosynthesis of 4MI3G and camalexin in defense against Bc.

中文翻译:


CPK5/CPK6 和 MPK3/MPK6 信号通路共同调节吲哚芥子油苷和camalexin生物合成。



以吲哚芥子油苷(IGS)和camalexin为代表的次生植物代谢产物在拟南芥免疫中发挥着重要作用。之前,我们证明了 MPK3 和 MPK6 这两种密切相关的 MAPK 在调节灰葡萄孢( Bc ) 诱导的 IGS 和camalexin 生物合成中的重要性。在这里,我们报道 CPK5 和 CPK6 这两种冗余的钙依赖性蛋白激酶 (CPK) 也参与调节这些次级代谢产物的生物合成。 CPK5CPK6的功能丧失会损害植物对Bc的抗性。 CPK5-VK转基因植物的表达谱(其中截短的组成型活性 CPK5 由类固醇诱导型启动子驱动)表明,IGS 和 camalexin 途径的生物合成基因在 CPK5-VK 诱导后协调上调,导致高camalexin 和 4-甲氧基吲哚-3-基-甲基芥子油苷 (4MI3G) 的水平积累。 camalexin 和 4MI3G 的诱导以及其生物合成途径中的基因在响应Bc 的cpk5 cpk6突变体中受到极大损害。在条件cpk5 cpk6 mpk3 mpk6四重突变体中,与cpk5 cpk6或条件mpk3 mpk6双突变体相比, Bc抗性以及 IGS 和 camalexin 的诱导进一步降低,表明 CPK5/CPK6 和 MPK3/MPK6 信号通路均有助于促进4MI3G 和 camalexin 的生物合成可防御Bc
更新日期:2020-05-25
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