| Autor: |
Lu, Jin Fang, Wang, Wei Na, Wang, Gai Ling, Zhang, He, Zhou, Ying, Gao, Zhi Peng, Nie, Pin, Xie, Hai Xia |
| Zdroj: |
Infection and Immunity; October 2015, Vol. 84 Issue: 1 p2-10, 9p |
| Abstrakt: |
ABSTRACTThe type III secretion system (T3SS) of Edwardsiella tardais crucial for its intracellular survival and pathogenesis in fish. The orf13gene (escE) of E. tardais located 84 nucleotides (nt) upstream of esrCin the T3SS gene cluster. We found that EscE is secreted and translocated in a T3SS-dependent manner and that amino acids 2 to 15 in the N terminus were required for a completely functional T3SS in E. tarda. Deletion of escEabolished the secretion of T3SS translocators, as well as the secretion and translocation of T3SS effectors, but did not influence their intracellular protein levels in E. tarda. Complementation of the escEmutant with a secretion-incompetent EscE derivative restored the secretion of translocators and effectors. Interestingly, the effectors that were secreted and translocated were positively correlated with the EscE protein level in E. tarda. The escEmutant was attenuated in the blue gourami fish infection model, as its 50% lethal dose (LD50) increased to 4 times that of the wild type. The survival rate of the escEmutant-strain-infected fish was 69%, which was much higher than that of the fish infected with the wild-type bacteria (6%). Overall, EscE represents a secreted T3SS regulator that controls effector injection and translocator secretion, thus contributing to E. tardapathogenesis in fish. The homology of EscE within the T3SSs of other bacterial species suggests that the mechanism of secretion and translocation control used by E. tardamay be commonly used by other bacterial pathogens. |
| Databáze: |
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