Cell wall integrity and high osmolarity glycerol pathways are required for adaptation of Alternaria brassicicola to cell wall stress caused by brassicaceous indolic phytoalexins
Cell wall integrity and high osmolarity glycerol pathways are required for adaptation of Alternaria brassicicola to cell wall stress caused by brassicaceous indolic phytoalexins
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DOI：
10.1111/j.1462-5822.2010.01520.x
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发表时间：
2011-01-01
影响因子：
3.4
通讯作者：
Simoneau, Philippe
中科院分区：
文献类型：
--
作者：
Joubert, Aymeric;Bataille-Simoneau, Nelly;Simoneau, Philippe
Camalexin是拟南芥特有的植物抗毒素，它对油菜链格孢的生长有抑制作用.这种植物代谢产物可能通过引起细胞膜损伤来发挥其抗真菌毒性。在这里，我们观察到，激活这种损伤的细胞反应需要细胞壁完整性（CWI）和高渗透压甘油（HOG）途径。发现Camalexin激活AbHog1和AbSlt2 MAP激酶，并且后者的激活在AbHog1缺陷型菌株中被废除。缺乏功能性MAP激酶的突变株表现出对camalexin和brassinin的超敏反应，camalexin和brassinin是由几种栽培芸苔属物种产生的结构相关的植物抗毒素。MAP激酶缺陷突变体对camalexin的膜透化活性的敏感性增强。这些结果表明，这两种信号通路在调节细胞代偿反应以在暴露于camalexin期间保持细胞完整性方面具有关键作用。AbHog1和AbSlt2缺陷型突变体对宿主植物的毒性降低，这可能至少对后者突变体而言，部分是由于它们无法科普防御代谢产物如吲哚植物抗毒素。这构成了植物抗毒素激活真菌MAP激酶和激活级联的输出有助于保护真菌对抗抗微生物植物代谢物的第一个证据。
P>Camalexin, the characteristic phytoalexin of Arabidopsis thaliana, inhibits growth of the fungal necrotroph Alternaria brassicicola. This plant metabolite probably exerts its antifungal toxicity by causing cell membrane damage. Here we observed that activation of a cellular response to this damage requires cell wall integrity (CWI) and the high osmolarity glycerol (HOG) pathways. Camalexin was found to activate both AbHog1 and AbSlt2 MAP kinases, and activation of the latter was abrogated in a AbHog1 deficient strain. Mutant strains lacking functional MAP kinases showed hypersensitivity to camalexin and brassinin, a structurally related phytoalexin produced by several cultivated Brassica species. Enhanced susceptibility to the membrane permeabilization activity of camalexin was observed for MAP kinase deficient mutants. These results suggest that the two signalling pathways have a pivotal role in regulating a cellular compensatory response to preserve cell integrity during exposure to camalexin. AbHog1 and AbSlt2 deficient mutants had reduced virulence on host plants that may, at least for the latter mutants, partially result from their inability to cope with defence metabolites such as indolic phytoalexins. This constitutes the first evidence that a phytoalexin activates fungal MAP kinases and that outputs of activated cascades contribute to protecting the fungus against antimicrobial plant metabolites.