Kaliff Maria, Staal Jens, Myrenås Mattias, Dixelius Christina
Department of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, P.O. Box 7080, 750 07 Uppsala, Sweden.
Mol Plant Microbe Interact. 2007 Apr;20(4):335-45. doi: 10.1094/MPMI-20-4-0335.
Abscisic acid (ABA) is a defense hormone with influence on callose-dependent and -independent resistance against Leptosphaeria maculans acting in the RLMcol pathway. ABA-deficient and -insensitive mutants in Ler-0 background (abal-3 and abil-1) displayed susceptibility to L. maculans, along with a significantly decreased level of callose depositions, whereas abi2-1 and abi3-1 remained resistant, together with the abi5-1 mutant of Ws-0 background. Suppressor mutants of abil-1 confirmed that the L. maculans-susceptible response was due to the dominant negative nature of the abil-1 mutant. Highly induced camalexin levels made ABA mutants in Col-0 background (aba2-1, aba3-1, and abi4-1) appear resistant, but displayed enhanced susceptibility as double mutants with pad3-1, impaired in camalexin biosynthesis. beta-Aminobutyric acid (BABA) pretreatment of Ler-0 contributed to an elevated level of endogenous ABA after L. maculans inoculation. Comparisons between (RLM1co1)pad3 and rlmlLerpad3 showed that ABA and BABA enhancement of callose deposition requires induction from RLM1col. ABII, but not ABI2, was found to be involved in a feedback mechanism that modulates RLM1co, expression. Genetic analysis showed further that this feedback occurs upstream of ABI4 and that components downstream of ABI4 modulate ABIJ activity. ABA and BABA treatments of the L. maculans-susceptible callose synthase mutant pmr4 showed that ABA also induces a callose-independent resistance. Similar treatments enhanced callose depositions and induced resistance to L. maculans in oilseed rape, and BABA-induced resistance was found to be independent of salicylic acid.
脱落酸（ABA）是一种防御激素，在RLMcol途径中对依赖胼胝质和不依赖胼胝质的抗黄斑盘多毛孢菌抗性有影响。Ler-0背景下的ABA缺陷型和不敏感型突变体（abal-3和abil-1）对黄斑盘多毛孢菌表现出易感性，同时胼胝质沉积水平显著降低，而abi2-1和abi3-1以及Ws-0背景下的abi5-1突变体仍具有抗性。abil-1的抑制突变体证实，对黄斑盘多毛孢菌的易感反应是由于abil-1突变体的显性负性性质。在Col-0背景下，高诱导的camalexin水平使ABA突变体（aba2-1、aba3-1和abi4-1）表现出抗性，但与camalexin生物合成受损的pad3-1双突变体一起时，表现出增强的易感性。用β-氨基丁酸（BABA）预处理Ler-0会导致接种黄斑盘多毛孢菌后内源性ABA水平升高。(RLM1co1)pad3和rlmlLerpad3之间的比较表明，ABA和BABA对胼胝质沉积的增强需要RLM1col诱导。发现ABII而非ABI2参与调节RLM1co表达的反馈机制。遗传分析进一步表明，这种反馈发生在ABI4上游，且ABI4下游的成分调节ABI1活性。对易感黄斑盘多毛孢菌的胼胝质合酶突变体pmr4进行ABA和BABA处理表明，ABA还诱导不依赖胼胝质的抗性。类似处理增强了油菜中的胼胝质沉积并诱导了对黄斑盘多毛孢菌的抗性，且发现BABA诱导的抗性不依赖于水杨酸。
