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首页> 外文期刊>Infection and immunity >Host Cell Contact-Induced Transcription of the Type IV Fimbria Gene Cluster of Actinobacillus pleuropneumoniae
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Host Cell Contact-Induced Transcription of the Type IV Fimbria Gene Cluster of Actinobacillus pleuropneumoniae

机译：宿主细胞接触诱导的胸膜肺炎放线杆菌IV型菌毛基因簇的转录。

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Type IV pili (Tfp) of gram-negative species share many characteristics, including a common architecture and conserved biogenesis pathway. Much less is known about the regulation of Tfp expression in response to changing environmental conditions. We investigated the diversity of Tfp regulatory systems by searching for the molecular basis of the reported variable expression of the Tfp gene cluster of the pathogen Actinobacillus pleuropneumoniae. Despite the presence of an intact Tfp gene cluster consisting of four genes, apfABCD, no Tfp were formed under standard growth conditions. Sequence analysis of the predicted major subunit protein ApfA showed an atypical alanine residue at position ?1 from the prepilin peptidase cleavage site in 42 strains. This alanine deviates from the consensus glycine at this position in Tfp from other species. Yet, cloning of the apfABCD genes under a constitutive promoter in A. pleuropneumoniae resulted in pilin and Tfp assembly. Tfp promoter-luxAB reporter gene fusions demonstrated that the Tfp promoter was intact but tightly regulated. Promoter activity varied with bacterial growth phase and was detected only when bacteria were grown in chemically defined medium. Infection experiments with cultured epithelial cells demonstrated that Tfp promoter activity was upregulated upon adherence of the pathogen to primary cultures of lung epithelial cells. Nonadherent bacteria in the culture supernatant exhibited virtually no promoter activity. A similar upregulation of Tfp promoter activity was observed in vivo during experimental infection of pigs. The host cell contact-induced and in vivo-upregulated Tfp promoter activity in A. pleuropneumoniae adds a new dimension to the diversity of Tfp regulation.
机译：革兰氏阴性菌种的IV型菌毛（Tfp）具有许多特征，包括共同的结构和保守的生物发生途径。关于响应于变化的环境条件调节Tfp表达的了解还很少。我们通过寻找病原体胸膜肺炎放线杆菌的Tfp基因簇的可变表达的分子基础，研究了Tfp调控系统的多样性。尽管存在由四个基因 apfABCD 组成的完整Tfp基因簇，但在标准生长条件下没有形成Tfp。预测的主要亚基蛋白ApfA的序列分析显示，在42株菌株中，从前毛蛋白肽酶切割位点的第1位非典型的丙氨酸残基。该丙氨酸与其他物种在Tfp中的该位置偏离共有甘氨酸。但是，在 A的组成型启动子下克隆了 apfABCD 基因。胸膜肺炎导致菌毛蛋白和Tfp的组装。 Tfp启动子- luxAB 报告基因融合表明，Tfp启动子是完整的但受到严格调控。启动子活性随细菌生长期而变化，仅在细菌在化学成分确定的培养基中生长时才能检测到。用培养的上皮细胞进行的感染实验表明，当病原体粘附到肺上皮细胞的原代培养物中时，Tfp启动子活性被上调。培养物上清液中的非粘附细菌实际上不显示启动子活性。在猪的实验性感染期间，体内观察到了类似的Tfp启动子活性上调。在 A中，宿主细胞接触诱导和体内上调的Tfp启动子活性。胸膜肺炎为Tfp调节的多样性增加了新的维度。

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