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在鲁氏耶尔森氏菌中克隆对蜂毒素 B 有反应的内切核酸酶。

Molecular cloning of cecropin B responsive endonucleases in Yersinia ruckeri.

机构信息

Department of Molecular and Cell Biology, University of Connecticut, 91 N. Eagleville Rd., U-3125, Storrs, CT 06269-3125, USA.

出版信息

Mar Biotechnol (NY). 2011 Feb;13(1):56-65. doi: 10.1007/s10126-010-9269-z. Epub 2010 Mar 30.

Abstract

We have previously demonstrated that Yersinia ruckeri resists cecropin B in an inducible manner. In this study, we sought to identify the molecular changes responsible for the inducible cecropin B resistance of Y. ruckeri. Differences in gene expression associated with the inducible resistance were investigated. Cultures of Y. ruckeri were exposed to a sublethal concentration of cecropin B and resultant changes in the messenger RNA population of the bacteria were assayed using the differential display reverse transcription polymerase chain reaction (DD-RT-PCR). A single band was consistently increased in intensity in all repeats of the experiment. The band was excised, cloned, sequenced, and used to screen a Y. ruckeri genomic DNA library. The DD-RT-PCR fragment shared 100% identity to the cDNA sequence of an ATP-dependent endonuclease of the overcome lysogenization defect (OLD) family of Y. ruckeri 29473. The genomic clone that was recovered was not identical to the DD-RT-PCR clone, but harbored a gene for a secreted endonuclease 1 (nucM) homologue. It was determined that transcription of the gene was upregulated following exposure to cecropin B via RT-PCR. Furthermore, an increase in the nuclease activity of culture supernatants of Y. ruckeri following exposure to cecropin B was demonstrated. These findings demonstrate that cecropin B exposure increases the expression of at least two endonucleases in Y. ruckeri. The production and secretion of an endonuclease by Y. ruckeri in response to an antimicrobial peptide indicates the involvement of both intracellular and extracellular DNA in the toxic effects of cecropin B.

摘要

我们之前已经证明了虹彩病毒属鱼类迟缓爱德华氏菌以可诱导的方式抵抗蜂毒素 B。在这项研究中,我们试图确定导致虹彩病毒属鱼类迟缓爱德华氏菌可诱导蜂毒素 B 抗性的分子变化。研究了与诱导抗性相关的基因表达差异。将虹彩病毒属鱼类迟缓爱德华氏菌的培养物暴露于亚致死浓度的蜂毒素 B 下,并使用差异显示逆转录聚合酶链反应 (DD-RT-PCR) 检测细菌的信使 RNA 群体的变化。在实验的所有重复中,一个条带的强度始终一致增加。该条带被切除、克隆、测序,并用于筛选虹彩病毒属鱼类迟缓爱德华氏菌 29473 的克服溶原缺陷 (OLD) 家族的 ATP 依赖性内切酶的基因组 DNA 文库。DD-RT-PCR 片段与该内切酶 cDNA 序列完全一致。回收的基因组克隆与 DD-RT-PCR 克隆不完全相同,但携带有一个分泌型内切酶 1 (nucM) 同源物的基因。通过 RT-PCR 确定,在暴露于蜂毒素 B 后,该基因的转录被上调。此外,还证明了在暴露于蜂毒素 B 后,虹彩病毒属鱼类迟缓爱德华氏菌的培养物上清液中的核酸酶活性增加。这些发现表明,蜂毒素 B 的暴露增加了虹彩病毒属鱼类迟缓爱德华氏菌中至少两种内切酶的表达。虹彩病毒属鱼类迟缓爱德华氏菌在受到抗菌肽的刺激时产生和分泌内切酶,表明细胞内和细胞外 DNA 都参与了蜂毒素 B 的毒性作用。

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