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研究生:蔡念培
研究生(外文):Nien-Pei Tsai
論文名稱:腸出血性大腸桿菌O157:H7之致病島嶼基因L0036的多重調控功能
論文名稱(外文):Multiple Functions of L0036 in Regulation of the Pathogenicity Island of Enterohemorrhagic Escherichia coli O157:H7
指導教授:許萬枝許萬枝引用關係
指導教授(外文):Wan-Jr Syu
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:微生物及免疫學研究所
學門:生命科學學門
學類:微生物學類
論文種類:學術論文
論文出版年:2004
畢業學年度:92
語文別:中文
中文關鍵詞:腸出血性大腸桿菌調控致病島嶼
外文關鍵詞:Enterohemorrhagic Escherichia coli O157:H7regulationLEE island
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出血性大腸桿菌與致病性大腸桿菌 (EPEC) 都屬於病原性的大腸桿菌,其感染人類腸內上皮細胞後會造成腸內微絨毛的破壞,引發嚴重的所謂 A/E lesion 病灶。一般來說,引發 A/E lesion 病原基因均來自於細菌基因組中一段被稱為 LEE island 的特殊區域,此區域共包含有 41 個開放閱讀框架 (open reading frame),而約可歸為五個主要的操縱子 (operon),分別為 LEE1、LEE2、LEE3、LEE4 與 tir (LEE5)。LEE island 的表現受到非常複雜的調控,就目前所知,在 LEE island 有兩個活化型調控蛋白 (Ler 與 GrlA) 與一個抑制型調控蛋白 (GrlR) 的存在 (Deng et al.),然而我們將在這裡引入一個尚未發表的調控性蛋白質 L0036。在已發表的文獻中,L0036 曾被推斷為形成第三型分泌系統的一個組成分子(Aizawa, 2001),不過在此我們發現 L0036 是個在 RNA 與 蛋白質層面的表現都受到嚴謹調控的基因,但 L0036 的表現與否並不影響第三型分泌系統的正常功能,然而 L0036 下游基因的轉譯卻又仰賴 L0036 的完整轉譯,可見其重要性;另外,當我們將 L0036 過量表現於 EHEC 中時,我們發現 L0036 會專一性的與 Ler 產生交互作用進而抑制 LEE island 的表現。由於 L0036 具有此多重功能,因此我們將 L0036 重新命名為 multiple-point controller (mpc) 而其基因產物則為 Mpc。
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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吳宜之 (2002) 從訊息核醣核酸及蛋白質層面分析出血性大腸桿菌O157:H7 致病島嶼,碩士論文,國立陽明大學微生物及免疫學研究所。
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