几丁质酶编码基因FolCTS3参与调控尖孢镰刀菌几丁质酶活性和致病力的研究

Chitinase gene FolCTS3 confers tomato wilt disease by effecting chitinase activity and pathogenicity in Fusarium oxysporum

番茄枯萎病是一种由尖孢镰刀菌番茄专化型(Fusarium oxysporum f.sp.lycopersici, Fol)引起的土传植物病害,严重影响番茄农业生产。几丁质酶(CTS)在丝状真菌中保守存在,在真菌细胞壁形成过程中起着关键作用,但是否参与尖孢镰刀菌的致病过程目前尚未见报道。在Fol中鉴定到2个几丁质酶编码基因FolCTS2和FolCTS3,利用基因敲除方法研究其在病原菌致病中的功能。结果表明:缺失FolCTS3不影响Fol菌丝生长及对非生物胁迫的耐受能力,但显著影响几丁质酶活性和致病力,其缺失突变体的几丁质酶活性和致病能力显著下降;而缺失FolCTS2对Fol生物学表型无显著影响。这一研究提示几丁质酶编码基因FolCTS3参与调控尖孢镰刀菌的几丁质酶活性和致病过程,为解析尖孢镰刀菌的致病分子机制及番茄枯萎病防治策略的制定提供了理论依据。

Tomato wilt disease,caused by Fusarium oxysporum f.sp.lycopersici(Fol),is the most devastating fungal disease and severely threats to tomato production.Chitinase(CTS)is conserved in radial fungi and plays a key role in the formation of fungal cell walls.However,the roles of chitinase in pathogenicity have not yet been characterized in fungal pathogens.In this study,two chitinase-encoding genes FolCTS2 and FolCTS3 were identified in Fol and characterized that chitinase contributed to pathogenic development by deletion FolCTSs in Fol.The results showed that the deletion of FolCTS3 did not impair the growth of mycelium and tolerance to abiotic stress,but showed the loss of chitinase activity and pathogenicity in FolCTS3 mutants.The deletion of FolCTS2 had no significant effects on the biological function in Fol.In conclusions,the chitinase gene FolCTS3 is involved in regulating the chitinase activity and pathogenic process in Fol.Our results unveil the pathogenic molecular mechanism of Fol,and provide a theoretical basis for controlling tomato wilt disease strategies.