Flors Victor, Ton Jurriaan, van Doorn Ronald, Jakab Gabor, García-Agustín Pilar, Mauch-Mani Brigitte
Laboratory of Molecular and Cellular Biology, Institute of Botany, University of Neuchâtel, Rue Emile-Argand 11, Case Postale 158, 2009 Neuchâtel, Switzerland.
Plant J. 2008 Apr;54(1):81-92. doi: 10.1111/j.1365-313X.2007.03397.x. Epub 2007 Dec 15.
We have examined the role of the callose synthase PMR4 in basal resistance and beta-aminobutyric acid-induced resistance (BABA-IR) of Arabidopsis thaliana against the hemi-biotrophic pathogen Pseudomonas syringae and the necrotrophic pathogen Alternaria brassicicola. Compared to wild-type plants, the pmr4-1 mutant displayed enhanced basal resistance against P. syringae, which correlated with constitutive expression of the PR-1 gene. Treating the pmr4-1 mutant with BABA boosted the already elevated levels of PR-1 gene expression, and further increased the level of resistance. Hence, BABA-IR against P. syringae does not require PMR4-derived callose. Conversely, pmr4-1 plants showed enhanced susceptibility to A. brassicicola, and failed to show BABA-IR. Wild-type plants showing BABA-IR against A. brassicicola produced increased levels of JA. The pmr4-1 mutant produced less JA upon A. brassicicola infection than the wild-type. Blocking SA accumulation in pmr4-1 restored basal resistance, but not BABA-IR against A. brassicicola. This suggests that the mutant's enhanced susceptibility to A. brassicicola is caused by SA-mediated suppression of JA, whereas the lack of BABA-IR is caused by its inability to produce callose. A. brassicicola infection suppressed ABA accumulation. Pre-treatment with BABA antagonized this ABA accumulation, and concurrently potentiated expression of the ABA-responsive ABI1 gene. Hence, BABA prevents pathogen-induced suppression of ABA accumulation, and sensitizes the tissue to ABA, causing augmented deposition of PMR4-derived callose.
我们研究了胼胝质合成酶PMR4在拟南芥对半活体营养型病原菌丁香假单胞菌和坏死营养型病原菌芸苔链格孢的基础抗性及β-氨基丁酸诱导抗性（BABA-IR）中的作用。与野生型植物相比，pmr4-1突变体对丁香假单胞菌表现出增强的基础抗性，这与PR-1基因的组成型表达相关。用BABA处理pmr4-1突变体可提高PR-1基因已经升高的表达水平，并进一步增强抗性。因此，对丁香假单胞菌的BABA-IR不需要PMR4衍生的胼胝质。相反，pmr4-1植物对芸苔链格孢表现出增强的易感性，并且未表现出BABA-IR。表现出对芸苔链格孢的BABA-IR的野生型植物产生了更高水平的茉莉酸（JA）。pmr4-1突变体在受到芸苔链格孢感染后产生的JA比野生型少。阻断pmr4-1中的水杨酸（SA）积累可恢复基础抗性，但不能恢复对芸苔链格孢的BABA-IR。这表明突变体对芸苔链格孢增强的易感性是由SA介导的对JA的抑制引起的，而缺乏BABA-IR是由于其无法产生胼胝质。芸苔链格孢感染抑制了脱落酸（ABA）的积累。用BABA预处理可拮抗这种ABA积累，并同时增强ABA响应基因ABI1的表达。因此，BABA可防止病原体诱导的ABA积累抑制，并使组织对ABA敏感，导致PMR4衍生的胼胝质沉积增加。
