腸道出血性大腸桿菌(Enterohaemorrhagic Escherichia coli , EHEC)是一種病原性大腸桿菌，會引起人體很嚴重的感染症狀，像是溶血性貧血和溶血性尿毒症候群。然而，在EHEC中，志賀毒素(shiga toxin, stx)是最主要的毒素因子，其基因位在潛在於細菌染色體中的類λ原噬菌體區域上。毒素的表現通常會跟被DNA損傷並藉由SOS反應途徑所引發的噬菌體誘導一起發生。在先前的文獻中顯示，AbpAB能夠阻止噬菌體的增殖，其中也包含了λ噬菌體。此篇研究將探討AbpAB是否能夠抑制在EHEC菌株，EDL933中的噬菌體增殖以及毒素的製造並且解析其中的機轉。當EHEC在受到mitomycin C (MMC)以及ciprofloxacin (CPFX)的誘導引發噬菌體以及毒素的產生之下，有表現AbpAB的組別，噬菌斑數量以及毒素的表現都有著顯著的下降。這結果顯示AbpAB抑制了在溶原性菌株中噬菌體的增殖。從生長曲線的實驗中也看到AbpAB能夠阻止在MMC和CPFX的作用底下EHEC菌株的裂解。另外在紙錠擴散法當中，有表現AbpAB的組別相較其他組而言，MMC造成的抑制圈比較大和螢光強度較弱。這代表SOS反應被AbpAB所抑制。為了進一步找到AbpAB的作用目標，我們做了LexA降解實驗。結果指出，AbpAB並沒有抑制LexA的降解，然而recA突變的組別則有。因此得知，AbpAB可能並不是作用在RecA上。根據先前文獻已知部分雙重突變的菌株(∆dam ∆recA, ∆dam ∆recB, ∆dam ∆recC)無法存活。因此我們將AbpAB利用轉型方式送進∆dam的菌株，發現了在∆dam中表現AbpAB時，細菌是能夠存活的。這代表了AbpAB不是作用在RecA、RecB、RecC這三個蛋白上。另外，三重突變(∆rep ∆recD ∆recA)的菌株也不能存活，然而他們當中雙重突變的卻能夠活。我們發現當在雙重突變(∆rep ∆recA)的菌株中表現AbpAB會使細菌無法生存，這現象跟三重突變的情況是類似的。根據這些結果，我們猜測AbpAB可能是作用在RecD上面。
這個研究顯示了在利用MMC和CPFX造成DNA損傷的情形下，AbpAB在大腸桿菌中能夠藉由抑制SOS反應進而阻止噬菌體的增殖。但還需要更進一步的研究去了解更加詳細的機轉。綜合上述，從此篇研究中所獲得的知識將有助於將來研發針對關於EHEC感染的策略。

Enterohaemorrhagic Escherichia coli (EHEC) cause the most severe E. coli infection with such as hemorrhagic colitis and hemorrhagic uremic syndrome (HUS). Shiga toxin is the major virulence factor during EHEC infection, and the gene encoding toxin is located on λ-like prophage region integrated into the bacterial chromosome. The expression of toxin is generally coupled to the phage induction through SOS response triggered by DNA damage. In a previous study showed that AbpAB can block the propagation of bacteriophages including λ phage. Here, we challenged whether AbpAB inhibits the phage propagation in E. coli o157:H7 EDL933, which is a model for EHEC, to prevent the toxin production and elucidate the mechanism. When the EHEC cells expressing AbpAB was cultured with mitomycin C (MMC) and ciprofloxacin (CPFX) to induce the phage and shiga toxin production, the plaque number and toxin level were decreased significantly. The result indicated that AbpAB inhibited phage production from the lysogenic strain. Growth curve of the strain showed that AbpAB prevented lysis of the EHEC strain under MMC and CPFX treatment. A disc diffusion test showed that inhibition zone of AbpAB expressing cells by MMC was bigger and its reporter signal was lower compared those without the expression. This result suggested that SOS response was blocked by AbpAB. To further elucidate the target of AbpAB, LexA degradation assay was performed to know whether RecA would be the target of AbpAB. As the result, AbpAB did not block the LexA degradation, while recA mutant did. Therefore, AbpAB might not target on RecA. It has been known that some doubled mutants (∆dam ∆recA, ∆dam ∆recB, ∆dam ∆recC) shows lethality. Thus, we transformed AbpAB plasmid into ∆dam strain and found that expression of AbpAB in ∆dam strain can grow. It indicated that AbpAB does not target on RecA, RecB, and RecC. Besides, a triple mutants strain (∆rep ∆recD ∆recA) also shows lethality, while the double mutants of them are survival. We found that a double mutant (∆rep ∆recA) expressing AbpAB showed lethality, and showed similar phenotype to the triple mutant. Based on these results, we suggested that AbpAB may target on RecD.
This study demonstrated that AbpAB inhibited phage production through blocking SOS response in E. coli, while DNA got damage by MMC or CPFX. But, further study is necessary to understand the molecular mechanism in detail. Together, the results of this research would be applicable to develop a treatment strategy for shiga toxin production in EHEC.

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