Beta-amino-butyric acid-induced resistance against necrotrophic pathogens is based on ABA-dependent priming for callose.
Beta-amino-butyric acid-induced resistance against necrotrophic pathogens is based on ABA-dependent priming for callose.
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发表时间：
2004
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通讯作者：
J. Ton;B. Mauch-Mani
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作者：
J. Ton;B. Mauch-Mani
非蛋白质氨基酸β-氨基丁酸（BABA）保护植物免受各种病原体的侵害。我们已经研究了BABA对两种坏死性病原体的抗性的有效性和作用方式。用BABA处理拟南芥，诱导对芸苔链格孢和黄瓜褐斑病菌的抗性达到茉莉酸（JA）的相似水平。相反，苯并噻二唑（BTH），水杨酸（SA）的功能类似物的治疗，对这两种病原体的抗性没有显着的影响。BABA诱导的对A.在JA不敏感突变体coi 1 -1和camalexin缺陷突变体pad 3 -1中，芸苔属和黄瓜疫霉不受影响。此外，ABA诱导的抗性的表达与camalexin的积累增强或JA诱导的PDF1.2基因的转录增强无关。在乙烯（ET）和SA信号转导受损的突变体中，ABA诱导的抗黄瓜疫霉的抗性的表达不受影响，但在脱落酸（阿坝）缺陷型突变体aba 1 -5、ABA不敏感型突变体abi 4 -1和胼胝质缺陷型突变体pmr 4 -1中被阻断。两种病原体感染后，ABA处理的植物表现出更早和更明显的胼胝质积累。用胼胝质抑制剂2-脱氧-D-葡萄糖（2-DDG）处理可逆转BABA诱导的对A.芸苔属。此外，引发的胼胝质沉积是不存在的ABA处理的abi 4 -1和pmr 4 -1植物感染后，由黄瓜疫霉。虽然ABA诱导的抗性的表达与ABA诱导的RAB 18基因的转录增强无关，但阿坝的应用模拟了BABA对胼胝质积累和抗性水平的影响。因此，ABA诱导的对坏死性病原体的抗性是基于引发的胼胝质积累，这是由ABA依赖性防御途径控制的。
The non-protein amino acid beta-amino-butyric acid (BABA) protects plants against a wide range of pathogens. We have examined the effectiveness and mode of action of BABA on resistance against two necrotrophic pathogens. Treatment of Arabidopsis with BABA induced resistance against Alternaria brassicicola and Plectosphaerella cucumerina to a similar level by jasmonic acid (JA). Conversely, treatment with benzothiadiazole (BTH), a functional analogue of salicylic acid (SA), had no significant effect on the resistance against both pathogens. BABA-induced resistance against A. brassicicola and P. cucumerina was unaffected in the JA-insensitive mutant coi1-1 and the camalexin-deficient mutant pad3-1. Moreover, the expression of BABA-induced resistance was not associated with enhanced accumulation of camalexin or enhanced transcription of the JA-inducible PDF1.2 gene. The expression of BABA-induced resistance against P. cucumerina was unaffected in mutants impaired in ethylene (ET) and SA signalling, but was blocked in the abscisic acid (ABA)-deficient mutant aba1-5, the ABA-insensitive mutant abi4-1 and the callose-deficient mutant pmr4-1. Upon infection by both pathogens, BABA-treated plants showed an earlier and more pronounced accumulation of callose. Treatment with the callose-inhibitor 2-deoxy-D-glucose (2-DDG) reversed the BABA-induced resistance against A. brassicicola. Furthermore, primed callose deposition was absent in BABA-treated abi4-1 and pmr4-1 plants upon infection by P. cucumerina. Although the expression of BABA-induced resistance was not associated with enhanced transcription of the ABA-inducible RAB18 gene, application of ABA mimicked the effect of BABA on the level of callose accumulation and resistance. Hence, BABA-induced resistance against necrotrophic pathogens is based on primed callose accumulation, which is controlled by an ABA-dependent defence pathway.