Degradation of oxalic acid by the mycoparasite Coniothyrium minitans plays an important role in interacting with Sclerotinia sclerotiorum
Degradation of oxalic acid by the mycoparasite Coniothyrium minitans plays an important role in interacting with Sclerotinia sclerotiorum
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真菌寄生虫 Coniothyrium minitans 对草酸的降解在与核盘菌的相互作用中发挥着重要作用
DOI：
10.1111/1462-2920.12409
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发表时间：
2014-08-01
影响因子：
5.1
通讯作者：
Li, Guo-Qing
中科院分区：
文献类型：
--
作者：
Zeng, Li-Mei;Zhang, Jing;Li, Guo-Qing
盾壳霉（Coniothyriumminitans，Cm）是由核盘菌（Sclerotiniaclerotiorum，Ss）寄生的一种真菌。SS产生的毒力因子草酸（OA），这是有毒的植物，也Cm，和Cm解毒OA降解。在这项研究中，两个草酸脱羧酶基因，Cmoxdc 1和Cmoxdc 2，克隆从Cm菌株Chy-1。OA和低pH诱导表达Cmoxdc 1，但不Cmoxdc 2。Cmoxdc 1部分负责OA降解，而Cmoxdc 2对OA降解没有影响。在CM中Cmoxdc 1的破坏降低了其在OA积累的双重培养物中感染Ss的能力。与Chy-1相比，Cmoxdc 1被破坏的突变体具有降低的两个真菌寄生虫相关基因几丁质酶（Cmch 1）和β-1，3-葡聚糖酶（Cmg 1）的表达水平，并且在OA存在下没有检测到胞外蛋白酶的活性。另一方面，Cmoxdc 1破坏的突变体在OA修正的培养基中的培养物显示出增强的抗真菌活性，这可能是因为在酸性pH条件下Cmoxdc 1介导的OA降解减少导致的抗真菌物质的产生增加。本研究提供了OA降解调节真菌寄生和寄生的CM对Ss的直接遗传证据，并揭示了复杂的策略，CM与代谢活跃的菌丝体和休眠的Ss的菌核相互作用。
Coniothyrium minitans (Cm) is a mycoparasite of the phytopathogenic fungus Sclerotinia sclerotiorum (Ss). Ss produces a virulence factor oxalic acid (OA) which is toxic to plants and also to Cm, and Cm detoxifies OA by degradation. In this study, two oxalate decarboxylase genes, Cmoxdc1 and Cmoxdc2, were cloned from Cm strain Chy-1. OA and low pH induced expression of Cmoxdc1, but not Cmoxdc2. Cmoxdc1 was partially responsible for OA degradation, whereas Cmoxdc2 had no effect on OA degradation. Disruption of Cmoxdc1 in Cm reduced its ability to infect Ss in dual cultures where OA accumulated. Compared with Chy-1, the Cmoxdc1-disrupted mutants had reduced expression levels of two mycoparasitism-related genes chitinase (Cmch1) and beta-1,3-glucanase (Cmg1), and had no detectable activity of extracellular proteases in the presence of OA. On the other hand, the cultural filtrates of the Cmoxdc1-disrupted mutants in OA-amended media showed enhanced antifungal activity, possibly because of increased production of antifungal substances under acidic pH condition resulted from reduced Cmoxdc1-mediated OA degradation. This study provides direct genetic evidence of OA degradation regulating mycoparasitism and antibiosis of Cm against Ss, and sheds light on the sophisticated strategies of Cm in interacting with metabolically active mycelia and dormant sclerotia of Ss.