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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/79350完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 廖淑貞(Shwu-Jen Liaw) | |
| dc.contributor.author | Wen-Yuan Lin | en |
| dc.contributor.author | 林文淵 | zh_TW |
| dc.contributor.author | f04424003 | |
| dc.date.accessioned | 2022-11-23T08:58:39Z | - |
| dc.date.available | 2021-11-03 | |
| dc.date.available | 2022-11-23T08:58:39Z | - |
| dc.date.copyright | 2021-11-03 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-10-27 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/79350 | - |
| dc.description.abstract | "奇異變型桿菌 (Proteus mirabilis)是主要造成泌尿道感染 (urinary tract infection, UTI)的病原菌之一，在長期使用尿導管的患者，容易造成伺機性感染。細菌為了適應環境，必須快速改變基因組表現， alternative sigma factors的功能便是因應外來環境變化，將轉錄組重新定向 (redirection)。RpoN為alternative sigma factors的一員，常與移動性、生物膜和尿素酶等細菌毒性因子相關，需要特定的enhancer binding proteins (EBPs)進行活化後，始能啟動轉錄。透過BLAST分析P. mirabilis N2 genome找出4個可能EBPs FhlA, QseF, PspF與NtrC，並挑選fhlA與qseF突變株分析重要毒性因子如尿素酶活性、移動性以及生物膜形成能力等。在尿素酶活性的部分，rpoN與fhlA突變株尿素酶活性顯著低於野生株；移動性的部分，rpoN及qseF突變株表面移行能力較野生株差；而生物膜形成能力上相較於野生株，qseF突變株則顯著低於野生株，而rpoN突變株則沒有明顯差異。 FhlA為formate hydrogenlyase (FHL)activator，擁有GAF domain來感受外界因子，可以活化的下游基因fdhF及hyf operon表現並形成FHL complex，FHL complex可以將生長環境去酸化。我們發現P. mirabilis N2尿素酶活性隨著pH值增加而增加，在pH9的時候達到最佳活性，因此我們假設FHL會協同尿素酶將環境去酸化，而使得尿素酶活性增加，實驗顯示隨著環境pH值增加到pH 9，hyfG及fhlA失去調控尿素酶活性的能力，而將野生株及hyfG突變株培養在pH 5人工尿中，發現hyf突變株去酸化的速度顯著低於野生株。我們利用人工尿模擬尿液環境，測試尿結石形成能力，可以看到hyfG及fhlA突變株尿結石形成能力顯著低於野生株。利用ICR母鼠泌尿道感染模型進行試驗，不論在膀胱或腎臟hyfG及fhlA突變株定殖能力皆顯著下降。 QseF為雙組成系統QseEF的response regulator，我們進行小鼠泌尿道感染試驗，發現qseF突變株定殖能力不論在膀胱或腎臟皆顯著低於野生株。 QseF正向調控glmY (sRNA)、flhDC (鞭毛調控轉錄因子)、cheA (化學趨化蛋白)以及負向調控rcsB (轉錄因子)等基因表現，其中QseF正向調控glmY基因轉錄，而GlmY可以直接與cheA mRNA作用，調控cheA的轉譯，進一步影響細菌移動性。 我們看到QseF正向調控glmZ及rpoS表現，而先前實驗室發現GlmZ透過正向調控rpoS表現可以幫助細菌抵抗酸性與氧化壓力環境，增加在巨噬細胞存活率，此外相對於野生株，qseEGF以及glmZ突變株對膀胱細胞侵入能力顯著下降。在本文我們也發現溶血素基因hpmAB表現量在qseF突變株中降低，同時qseF突變株對於膀胱細胞毒性也顯著低於野生株。 除了移動性、壓力抗性以及細胞毒性之外，QseF同時調控了生物膜的形成，利用螢光顯微鏡可以觀察到24小時qseF突變株生物膜呈網狀分布，而野生株則能聚集發展。我們將時間細分為2小時一個單位，監測生物膜形成的量，可以發現在8小時之前(含)，qseF突變株生物膜形成量大於野生株，而10小時開始qseF突變株生物膜量維持不變而野生株持續增加，以至於24小時顯著低於野生株。RNA-seq資料及qPCR確認，可以看到zapABCD蛋白酶相關基因在qseF突變株中較野生株下降，並利用qPCR發現QseF在24h時正向調控sRNA RyhB3、RprA以及alternative sigma factor RpoE，先前文獻顯示P. mirabilis生物膜相關纖毛MR/P受RpoE調控，在qPCR中發現RyhB3正向調控zapA, rpoE以及mrpA；RprA則正向調控mrpA。我們測試生物膜相關因子發現qseF突變株自聚集及細胞貼附能力較野生株上升，而僅有蛋白酶活性下降，因此我們認為蛋白酶為生物膜發展所必需，影響生物膜繼續發展，而受RpoE調控的MR/P纖毛在排除自聚集以及細胞貼附能力之外，仍然為生物膜生成之重要因子。 本研究我們發現了RpoN相關EBPs FhlA及QseF能調控移動性、尿素酶活性、生物膜形成能力等重要致病因子，我們推論一、在開始形成extracellular cluster時RpoN-FhlA調控FHL表現並與尿素酶協同作用，加速環境去酸化使礦物質結晶沉積，進一步形成感染性尿結石及生物膜。二、在細菌懸浮時QseF受尿素及油酸(oleic acid)抑制，使得纖毛表現上升，鞭毛表現下降，一方面增加細菌貼附細胞能力，另一方面減少鞭毛抗原躲避宿主免疫反應；三、在遇到固態表面時，油酸則從負向調控轉為正向調控QseF，QseF正向調控細菌移動性，使P. mirabilis可以上行感染、促進細菌侵入宿主細胞，躲避免疫反應、增加細胞毒性，以獲取更多養分、增加細菌壓力抗性，以提高被巨噬細胞吞噬後的存活率。綜合上述，P. mirabilis利用FhlA及QseF進行整體轉錄組的調控，使細菌可以迅速改變其轉錄組，以利在環境多變的泌尿道感染中生存。 " | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-23T08:58:39Z (GMT). No. of bitstreams: 1 U0001-2610202116184800.pdf: 5512748 bytes, checksum: b4b80bef980fe0f7c0272e67704ae41f (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | "口試委員會審定書 i 誌謝 ii 摘要 iii Abstract vi 目錄 ix 圖目錄 xiii 表目錄 xiv 第一章 緒論 1 第一節 奇異變形桿菌 (Proteus mirabilis)介紹 1 1.1 P. mirabilis的基本介紹 1 1.2 P. mirabilis與尿石症(urolithiasis) 1 1.3 P. mirabilis的細胞毒性與組織病理 1 1.4 P. mirabilis的毒性因子 2 1.4.1 鞭毛 (flagella) 3 1.4.2 生物膜 (biofilm) 3 1.4.3 尿素酶(urease) 3 1.4.4 溶血素 (haemolysin) 4 1.4.5 Proteus toxic agglutinin (Pta) 4 1.4.6 胺基酸分解酶 (deaminase) 5 第二節 RpoN (σN)與其相關enhancer binding proteins (EBPs)簡介 5 2.1 RpoN介紹 5 2.2 RpoN相關EBPs介紹 6 2.2.1 FhlA與formate hydrogenlyase complex 6 2.2.2 QseF 7 2.3 研究動機與目的 8 第二章 實驗材料與方法 9 第一節 實驗流程 9 第二節 實驗方法 9 2.1 實驗菌株與質體 9 2.2 實驗培養環境及培養基 11 2.3 生物資訊分析 11 2.3.1 生物資訊網站 11 2.3.2 生物資訊軟體 12 2.4 構築質體與突變株 (Construction of plasmids and P. mirabilis mutants) 13 2.4.1 構築突變株（Construction of mutant strain） 13 2.4.2 基因體DNA萃取（Genomic DNA extraction） 13 2.4.3 聚合酶連鎖反應（Polymerase chain reation，PCR） 14 2.4.4 限制酶酶切（Restriction enzyme digestion） 14 2.4.5 DNA純化（DNA purification） 14 2.4.5.1 直接純化DNA或PCR產物 14 2.4.5.2 切膠純化DNA或PCR產物 15 2.4.6 質體DNA萃取（Plasmid DNA extraction） 15 2.4.7 DNA黏合作用（DNA ligation） 15 2.4.7.1 DNA ligation 16 2.4.7.2 TA cloning 16 2.4.8 構築過度表達株（Construction of overexpression strain） 16 2.4.9 構築定點突變株（Construction of site-direct mutagenesis strain） 17 2.4.10 質體DNA轉型作用（Transformation） 17 2.4.10.1 電穿孔勝任細胞製備 17 2.4.10.2 電穿孔轉型 17 2.4.10.3 化學法勝任細胞製備 18 2.4.10.4 化學法轉型 18 2.4.11 細菌接合生殖（Conjugation） 18 2.4.12 南方墨點法（Southern blot analysis） 19 2.4.13 核酸定序與序列分析（Sequencing） 20 2.4.13.1 核酸定序 20 2.4.13.2 序列分析 20 2.5 基因表達 20 2.5.1 Promoter活性分析（Transcriptional reporter） 20 2.5.2 轉譯活性分析 (Translational reporter) 21 2.5.3 RNA萃取（RNA extraction） 22 2.5.4 RNA反轉錄（Reverse transcription） 22 2.5.5 同步定量PCR（Real-time PCR） 23 2.5.6 反轉錄PCR（RT-PCR） 23 2.6 蛋白質分析 23 2.6.1 鞭毛萃取（Flagellin extraction） 23 2.6.2 蛋白質濃度測定（Bio-Rad protein assay） 24 2.6.3 不連續膠體電泳（SDS-PAGE） 24 2.6.4 西方墨點法（Western blot） 25 2.7 抗藥性與壓力抗性 25 2.7.1 生長曲線（Growth curve） 25 2.7.2 最小抑制濃度（Minimum inhibitory concentration，MIC） 26 2.7.3 抗氧化壓力（Oxidative stress resistance） 26 2.7.4 抗酸性（Acid resistance） 26 2.8 生物膜 27 2.8.1 生物膜形成能力 (Biofilm formation ability) 27 2.8.2 時程生物膜形成能力 (Time-course biofilm formation ability) 27 2.8.3 細胞外多醣體測定 (Quantify exopolysaccharide (EPS)) 27 2.8.4 細胞外去氧核醣核酸測定 (Quantify extracellular DNA (eDNA)) 28 2.8.5 細胞疏水性 (Cell hydrophobicity) 28 2.8.6 細胞自聚合能力 (Cell autoaggregation) 28 2.9 移動性 29 2.9.1 表面移行（Swarming） 29 2.9.2 泳動（Swimming） 29 2.9.3 溶血素活性（Hemolysin activity） 29 2.10 尿素酶 29 2.10.1 尿素酶活性（Urease activity） 29 2.10.2 尿結石形成能力 (Urinary stone formation ability) 30 2.11 小鼠泌尿道感染 30 第三章 實驗結果 31 第一節 RpoN and EBPs in P. mirabilis 31 1.1 RpoN與EBPs突變株建構 31 1.2 生理、致病力及壓力抗性的影響 33 第二節 FhlA in P. mirabilis 35 2.1 FhlA在P. mirabilis N2中穩定表現不受氧氣及formate影響 35 2.2 FhlA在P. mirabilis N2調控的基因 37 2.3 Hydrogenase-4 (Hyf)在P. mirabilis的調控 39 2.4 RpoN-FhlA-Hyf增加P. mirabilis抗酸能力 41 2.5 RpoN-FhlA-Hyf促進P. mirabilis尿素酶活性 46 2.6 RpoN-FhlA-Hyf促進P. mirabilis 對ICR小鼠泌尿道的感染 49 第三節 QseF in P. mirabilis 50 3.1 QseF與sRNA GlmY對細菌移動性之調控 52 3.1.1 qseF與glmY共用promoter且受QseF調控 52 3.1.2 QseF與GlmY正向調控移動性相關表現型 54 3.1.3 QseF與GlmY正向調控flhDC與cheA表現並負向調控rcsB表現 56 3.1.4 GlmY與cheA mRNA interaction增加cheA mRNA translation效率 58 3.2 QseF對細菌壓力抗性與細胞毒性之調控 62 3.3 QseF對於生物膜形成之調控 64 3.3.1 QseF抑制生物膜初始貼附但為生物膜成熟所必須 64 3.3.2 QseF調控mrp, pmf以及cfa纖毛基因表現 65 3.3.3 QseF與ZapABCD 69 3.3.3.1 QseF促進蛋白酶活性 69 3.3.3.2 QseF正向調控蛋白酶相關操作組ZapABCD 70 3.3.3.3 QseF調控ZapABCD影響生物膜成熟而不是生物膜初始貼附 70 3.3.3.4 QseF不是在轉錄層級調控zapABCD表現 71 3.3.4 QseF與sRNA 73 3.3.4.1 QseF調控sRNA RprA以及RyhB3 73 3.3.4.2 sRNA RprA正向調控mrpA表現並促進P. mirabilis生物膜形成 73 3.3.4.3 sRNA RyhB3正向調控mrpA與zapA表現並促進P. mirabilis生物膜形成 74 3.3.5 QseF的訊號因子 76 第四章 結論 79 第五章 討論 80 第一節 FhlA在P. mirabilis泌尿道感染扮演的角色 80 第二節 FHL在P. mirabilis的表現 81 第三節 氫離子消耗型(proton consuming acid resistance)抗酸機制與尿素酶活性關係 82 第四節 QseF在P. mirabilis泌尿道感染扮演的角色 82 4.1 QseF調控sRNA GlmY與移動性 83 4.2 QseF調控壓力抗性 83 4.3 QseF調控生物膜形成 84 第五節 QseF、RNaseE adapter protein RapZ與sRNA的交互作用 87 參考文獻 89 附錄 100 附錄一、P. mirabilis致病因子 100 附錄二：P. mirabilis因具有許多致病因子，而導致上泌尿道的感染 101 附錄三：P. mirabilis在固體培養基上的表面移行 (swarming) 週期。 101 附錄四、A schematic model for formate hydrogenlyase 2 (FHL-2) complex 102 附錄五、Model of initial bladder colonization and cluster development by P. mirabilis. 102" | |
| dc.language.iso | zh-TW | |
| dc.title | 探討σ因子 RpoN的 兩個增強子結合蛋白FhlA以及QseF在奇異變形桿菌中所扮演的角色 | zh_TW |
| dc.title | The roles of two enhancer binding proteins FhlA and QseF of sigma factor RpoN in uropathogenic Proteus mirabilis | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 賴信志(Hsin-Tsai Liu),楊翠青(Chih-Yang Tseng),邱浩傑,蘇伯琦 | |
| dc.subject.keyword | 尿道致病性奇異變形桿菌,FhlA,HyfG,尿素酶活性,QseF,RpoN,毒力因子, | zh_TW |
| dc.subject.keyword | uropathogenic Proteus mirabilis,FhlA,HyfG,urease activity,QseF,RpoN,virulence factor, | en |
| dc.relation.page | 102 | |
| dc.identifier.doi | 10.6342/NTU202104245 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2021-10-28 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 醫學檢驗暨生物技術學研究所 | zh_TW |
| 顯示於系所單位： | 醫學檢驗暨生物技術學系 | |
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