摘要
为了确定编码迟缓爱德华氏菌(E.tarda)Ⅲ型分泌系统(T3SS)装置蛋白的esaC基因的功能,采用基因敲除的方法构建了E.tarda野生型致病菌株LSFAO的esaC基因无极性缺失突变株LSE40ΔesaC,该突变株缺失了esaC的46-1452bp。Western blotting分析表明,由于esaC的缺失,E.tarda T3SS的输送器蛋白(EseB,EseC,EseD)不能分泌到细胞外,同时细菌的自凝聚现象消失;毒力检测发现,突变株LSE40ΔesaC对蓝曼龙鱼的半数致死量比野生型菌株提高了11.5倍。结果表明,esaC基因影响T3SS输送器蛋白的分泌和E.tarda的毒力。此研究确定了esaC基因作为E.tarda T3SS装置蛋白的功能,加深了对E.tarda致病机理的了解。
In order to determine the function of the esaC gene encoding an apparatus protein of the type III secretion system (T3SS) of Edwardsiella tarda, the authors construct a AesaC mutant of a pathogenic E. tarda strain ISE40 by an inframe deletion method. In the mutant nucleotides of 46-1452bp of esaC is deleted. The western blotting analysis shows that the AesaC mutant does not secrete the translocator proteins (EseB, EseC and EseD) of E. tarda T3SS into the culture medium. Further investigation shows that the AesaC mutant does not autoaggregate in the culture medium. The LDs0 (50% lethal dose) of the △esaC mutant is shown about 11.5 times higher than that of the wild-type E. tarda in the infection experiments of the blue gourami ( Trichogazter trichopterus ). These results indicate that esaC affects the secretion of T3SS translocator proteins and the virulence of E. tarda.
出处
《高技术通讯》
EI
CAS
CSCD
北大核心
2010年第2期199-203,共5页
Chinese High Technology Letters
基金
863计划(2006AA100310)
国家自然科学基金(30671613)
青岛市科技发展计划(08-1-7-2-HY)资助项目