Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/22037
標題: 十字花科黑腐病菌的β-lactamase 表現之調控
Regulation of β-lactamase of Xanthomonas campestris pv. campestris 17
作者: 陳巨威
Chen, Jyu-Wei
關鍵字: Xanthomonas camprstris pv. campestris
十字花科黑腐病菌
Clp
β-lactamase
調控
出版社: 分子生物學研究所
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摘要: 格蘭氏陰性的 Xanthomonas camprstris pv. campestris 為十字花科蔬菜黑腐病菌,大多的 XCC 都有抵抗 β-lactam 類抗生素的能力,其抵抗的方式是表現出 β-lactamase 去分解 β-lactam 類抗生素。在許多格蘭氏陰性菌 genome 中,大多都有 ampR-bla system並且此系統為當接受到抗生素時才會誘導表現 β-lactamase,但已知在 Xc17 中此系統會持續表現 β-lactamase(XCC3039)。目前了解 Clp (cAMP receptor protein-like protein) 為 global transcription factor,而前人利用蛋白質二維電泳分析 P20H 及 P20H clp 突變株的胞外蛋白,觀察到 wild type 的 β-lactamase (XCC3039) 蛋白量多於 clp 突變株;而 He. Y. W. 在 2007 年發表利用生物晶片分析在 Xc1 中受 Clp 調控的基因,其中有 β-lactamase 受到正向調控,但其調控的基因和前人證實的不同。在 β-lactamase activity 測試中觀察到 TC817 (Xc17 clp mutant 株) 在無 ampicillin 的環境下,其活性近乎喪失;而在 TC817 培養基中添加 ampicillin,其活性提高約30倍,但其提高的活性仍只有 Xc17 β-lactamase activity 的 0.3 倍;而在 MIC 的結果中指出 TC817 對 beta-lactame 類抗生素抗性下降,因此更為確定 Clp 會去影響到 beta-lactamase 的表現量並且令原本為持續表現型轉變為誘導型。在 ampR-bla 之間的啟動子區域,發現到 60% 相似度的 CBS (Clp-Binding Site),在 gel retardation 的實驗中證實 Clp 結合在此啟動子區域 ; 而在TC817的 ampR 及 bla 啟動子活性上,在培養基中含有 ampicillin 其ampR 啟動子活性稍微提高在未含 ampicillin 的培養基中所測得的活性,但其 bla 的啟動子活性無差異。而在 Western blotting 結果中,觀察在Xc17中 Bla 蛋白表現不論是否在培養基中含有 ampicillin,其蛋白均會表現,並在生長速率上也無差異;而在 TC817 中當培養基含有 ampicillin 才會被誘導表現beta-lactamase,並在生長上 ampicillin 會造成 TC817 生長減緩。證實 Clp 會直接影響bla的表現,但是否有其它因子參與在之中仍尚探討。 .
Most of Xanthomonas camprstris pv. campestris(Xcc) have ability that they resisted beta-latam antibiotic. Most of Xcc destroyed beta-latam antibiotic by beta-lactamase. In genome of many germ negative bacteria, they existed ampR-bla system genes. When ampicillin existed in environment, the system is only induced and produced beta-lactamase. Although, Genome of Xc17 exist the system, but the system expressed beta-lactamase(XCC3039) continuously. Clp(cAMP receptor protein-like protein) is global transcription factor. Extracellular protein between P20H and P20H clp mutant analyzed by protein 2-D electrophoresis. The result express more Bla(XCC3039)protein of P20h than Bla protein of P20h clp mutant. However, in 2007 He. published the Bla protein(XCC2873) was regulated positively by Clp in XC1. But He's result is different with result of predecessor's experiment. In beta-lactamase activity, TC817 (Xc17 clp mutant) loss activity in medium without ampicillin. however, when medium include ampicillin, the beta-lactamse activity is induced in TC817.The activity is enhance 30 folds approximately when medium is added ampicillin. In MIC test, resistance of beta-lactam antibiotic of TC817 reduced. Therefore, Clp effected continuous expression of Bla protein in Xc17.Promoter region between bla and ampR excite 60 percents of Clp-Binding Site(CBS).In gel retardation, tre result that Clp can bind this region is confirmed. In promoter activity assay, when medium included ampicillin, the activity of promoter region of ampR in TC817 was enhanced slightly. But the activity of promoter region of bla in TC817 was not different. In Western blotting assay, when medium included ampicillin in Xc17, Bla protein was still monitored and growth rate was also not different. However, when medium only included ampicillin in TC817, Bla protein was just monitored and growth rate was suppressed.
URI: http://hdl.handle.net/11455/22037
其他識別: U0005-1708200918271700
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