Type II secretion and type IV pili of Francisella
Type II secretion and type IV pili of Francisella
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DOI：
10.1196/annals.1409.016
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发表时间：
2007-01-01
期刊：
影响因子：
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通讯作者：
Guina, Tina
中科院分区：
文献类型：
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作者：
Forsberg, Ake;Guina, Tina
图拉氏弗朗西斯菌基因组编码IV型菌毛的同源物。尽管TFP表达所需的几个图拉氏F菌基因与11型分泌物(T2S)所需的基因同源，但这些基因簇主要具有典型的TFP结构特征。有初步证据表明，不同的图拉氏亚种表达类似TFP的表面结构，但亚种之间也存在一些有趣的差异。非致病亚种novicida(F.novicida)和高致病性A型毒株之间的一个区别是预测的PilA基因的序列不同。相比之下，B型菌株与A型菌株相比表现出一些差异，预测的两个Pilin基因和PILT基因是假基因，而Pila与A型菌株编码的Pila完全相同。这可能是有意义的，因为PilA有助于B型菌株的毒力，而PILT对于其他细菌病原体的TFP收回是必不可少的。TFP介导的蛋白质分泌只有在体外培养的F.novicida中才明显。令人惊讶的是，几种新城疫霉菌蛋白的分泌依赖于Pila和其他被认为在TFP表达中起作用的基因。在小鼠感染模型中，新城疫霉菌分泌物突变株的毒力更强。因此，在novicida中，TFP基因簇同时服务于T2S和TFP组装，人们很容易推测，致病亚种的进化涉及通过PilA和其他基因的结构变化而导致功能T2S的丧失，包括那些编码一些TFP分泌蛋白的基因。
Francisella tularensis genomes encode homologues of type IV pili. Though several F. tularensis genes required for Tfp expression are homologous to genes required for type 11 secretion (T2S), these gene clusters mainly bear structural signatures that are typical of Tfp. There is preliminary evidence that different F. tularensis subspecies express Tfp-like surface structures, but there are also some interesting differences between the subspecies. One difference between the nonpathogenic subspecies novicida (F. novicida) and the highly pathogenic type A strains is in sequence of one of the predicted pilin genes, pilA. In contrast, type B strains show several differences compared to type A strains, two predicted pilin genes and the pilT gene are pseudogenes, while pilA is identical to pilA that is encoded by the type A strains. This is likely significant as PilA contributes to virulence of type B strains while PilT is essential for Tfp retraction in other bacterial pathogens. Tfp-mediated protein secretion is only evident in in vitro grown F. novicida. Surprisingly, secretion of several F. novicida proteins was dependent on pilA and other genes with postulated roles in Tfp expression. F. novicida secretion mutants were more virulent in the mouse infection model. Thus, in F. novicida, Tfp gene clusters serve both T2S and Tfp assembly and it is tempting to speculate that evolution of the pathogenic subspecies involved loss of functional T2S via structural changes of PilA and additional genes, including those that encode some of the Tfp-secreted proteins.