| Summary: | 碩士 === 國立陽明大學 === 微生物及免疫學研究所 === 92 === Diarrheagenic enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) attach to human intestinal epithelium and efface brush border microvilli, forming A/E lesions. These human pathogens are phenotypically similar to the mouse pathogen Citrobacter rodentium. Genetically, they all have a homologous set of virulent genes involved in the A/E lesion, and these genes are organized on a locus of enterocyte effacement (Deng et al.), a pathogenicity island. The LEE island comprises 41 specific open reading frames (orfs), of which most are organized in five operons, LEE1, LEE2, LEE3, LEE4, and tir (LEE5). The expression of the LEE genes is regulated in a complicated manner, and current knowledge is that there are at least two positive regulators, Ler and GrlA, and one negative regulator, called GrlR. In EHEC, GrlA is encoded by L0043 whereas GrlR is encoded by L0044. In this thesis, we report a third regulatory gene located in LEE3, i.e., orf L0036 in EHEC. In the previous studies, L0036 has been implicated to function as a component of TTSS since the corresponding mutant phenotypically behaved as those with deletion of other orfs on the same operon or on LEE2. In addition to this observation, we found its expression was tightly controlled at both mRNA and protein levels. When overexpressed, this factor, named Mpc, interacted with Ler and suppressed the expression of the LEE proteins. When the translation wass not initiated or terminated before maturation, the type III secretion of effectors was completely abolished. Therefore, L0036 appeared to have multiple functions in addition to the fact that several cis elements reside on the region where L0036 spans.
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