Multiple contributions of peroxisomal metabolic function to fungal pathogenicity in Colletotrichum lagenarium
Multiple contributions of peroxisomal metabolic function to fungal pathogenicity in Colletotrichum lagenarium
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DOI：
10.1128/aem.00988-06
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发表时间：
2006-09-01
影响因子：
4.4
通讯作者：
Takano, Yoshitaka
中科院分区：
文献类型：
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作者：
Asakura, Makoto;Okuno, Tetsuro;Takano, Yoshitaka
在黄瓜炭疽病病原炭疽菌lagenarium中，PEX6是过氧化物酶体生物生成和附着胞介导的感染所必需的。为了验证过氧化物酶体相关代谢在真菌致病性中的作用，我们分离并功能表征了C lagenarium的ICL1，它编码参与过氧化物酶体中glyoxylate循环的异柠檬酸裂解酶。icl1突变体不能利用脂肪酸和醋酸酯来生长。虽然Icl1没有典型的过氧化物酶体靶向信号，但GFP-Icl1融合蛋白的表达分析表明，Ici1定位于过氧化物酶体。这些结果表明，在过氧化物酶体内部发生的乙醛酸循环是生长所需的脂肪酸和醋酸代谢所必需的。重要的是，与pex6突变体形成非黑色素化的附着胞相比，icl1突变体形成了黑色素高度着色的附着胞，这表明glyoxylate循环对于附着胞中的黑色素生物合成不是必需的。然而，icl1突变体表现出严重的毒力降低。icl1突变体的附着胞未能在寄主植物中发育穿透菌丝，表明icl1参与了寄主入侵。葡萄糖的加入部分恢复了icl1突变体的毒力。寄主植物的热休克处理也使icl1突变体产生病变，这表明icl1突变体的感染缺陷与植物防御有关。结合PEX6对附着体黑色素化的要求，我们的研究结果表明，过氧化物酶体代谢途径在附着体黑色素化和随后的宿主入侵步骤中发挥功能作用，而后者需要glyoxylate循环。
In Colletotrichum lagenarium, which is the causal agent of cucumber anthracnose, PEX6 is required for peroxisome biogenesis and appressorium-mediated infection. To verify the roles of peroxisome-associated metabolism in fungal pathogenicity, we isolated and functionally characterized ICL1 of C lagenarium, which encodes isocitrate lyase involved in the glyoxylate cycle in peroxisomes. The icl1 mutants failed to utilize fatty acids and acetate for growth. Although Icl1 has no typical peroxisomal targeting signals, expression analysis of the GFP-Icl1 fusion protein indicated that Ici1 localizes in peroxisomes. These results indicate that the glyoxylate cycle that occurs inside the peroxisome is required for fatty acid and acetate metabolism for growth. Importantly, in contrast with the pex6 mutants that form nonmelanized appressoria, the icl1 mutants formed appressoria that were highly pigmented with melanin, suggesting that the glyoxylate cycle is not essential for melanin biosynthesis in appressoria. However, the icl1 mutants exhibited a severe reduction in virulence. Appressoria of the icl1 mutants failed to develop penetration hyphae in the host plant, suggesting that ICL1 is involved in host invasion. The addition of glucose partially restored virulence of the icl1 mutant. Heat shock treatment of the host plant also enabled the icl1 mutants to develop lesions, implying that the infection defect of the icl1 mutant is associated with plant defense. Together with the requirement of PEX6 for appressorial melanization, our findings suggest that peroxisomal metabolic pathways play functional roles in appressorial melanization and subsequent host invasion steps, and the latter step requires the glyoxylate cycle.