中文摘要：

前期蛋白质组学研究发现尖孢镰刀菌古巴专化型4号生理小种（Foc4）中的过氧化氢酶1（cat1）基因受到巴西蕉诱导上调表达,为研究cat1基因在Foc4侵染香蕉过程中的作用,利用同源重组方法敲除Foc4的cat1基因,并对获得的敲除突变体开展表型分析和致病性测定。结果表明：cat1基因缺失对Foc4的菌丝、孢子形态、菌落生长、抗渗透压胁迫和细胞壁选择性压力等没有影响;但引起菌株抵抗外源氧胁迫、细胞壁穿透能力、纤维素利用能力减弱和对巴西蕉的致病性减弱。显示cat1基因的产物通过清除香蕉分泌的活性氧在Foc4对香蕉的致病过程中起作用,并参与病原菌对寄主纤维素成分的代谢。此结果为进一步深入研究香蕉枯萎病菌的致病机理奠定基础。

英文摘要：

It was found that the cat1 gene in Fusarium oxysporum Slx cubense race 4 （Foc4） was up-regulated induced by Musa sp. AAA. cv. Baxi in our previous proteomics analysis. In order to investigate the function of catl during the host infection process of Foc4, the carl gene in Foc4 was deleted by the homologous recombination method. The phenotype and pathogenicity of the carl knockout mutants were then analyzed. The results indicated that there were no apparent difference between the mutants and the wild type strain on mycelium and spores morphology, colonial growth, osmotic stress resistance and cell wall selective pressure. However, the mutants showed significant decrease in the abilities of exogenous oxygen stress resistance, penetrability of cell wall, cellulose utilization, and the pathogenicity to Musa spp. AAA. cv. Baxi. These results suggested that the carl gene in Foc4 should be involved in pathogenesis by scavenging host-derived ROS, and participated in the process of host cellulose degradation.