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鼠伤寒沙门氏菌侵袭基因invF和invG编码AraC和PulD蛋白家族的同源物。

The Salmonella typhimurium invasion genes invF and invG encode homologues of the AraC and PulD family of proteins.

作者信息

Kaniga K, Bossio J C, Galán J E

机构信息

Department of Microbiology, School of Medicine, State University of New York at Stony Brook 11794-5222.

出版信息

Mol Microbiol. 1994 Aug;13(4):555-68. doi: 10.1111/j.1365-2958.1994.tb00450.x.

DOI:10.1111/j.1365-2958.1994.tb00450.x
PMID:7997169
Abstract

We have identified two novel Salmonella typhimurium genes, invF and invG, which are required for the efficient entry of these organisms into cultured epithelial cells. invF and invG are located immediately upstream of invE, a previously identified gene also required for Salmonella entry. Non-polar mutations in these genes rendered S. typhimurium severely deficient for entry into cultured epithelial cells. The nucleotide sequences of invF and invG indicated that these genes encode polypeptides with predicted molecular weights of 24,373 and 62,275, respectively. Proteins of similar sizes were observed when invF and invG were expressed in a bacteriophage T7 RNA polymerase-based expression system. Comparison of the predicted sequence of InvF with translated sequences in the existing databases indicated that this protein is homologous to members of the AraC family of prokaryotic transcription regulators. However, mutations in invF did not significantly affect the expression of other members of the inv locus. InvG was found to be homologous to members of the PulD family of specialized translocases. This homology suggests that InvG may be necessary for the export of invasion-related determinants or involved in the assembly of a supramolecular structure that promotes entry.

摘要

我们鉴定出了两个新的鼠伤寒沙门氏菌基因,invF和invG,这些细菌高效进入培养的上皮细胞需要这两个基因。invF和invG位于invE的紧邻上游,invE是先前鉴定出的沙门氏菌进入细胞也需要的一个基因。这些基因中的非极性突变使鼠伤寒沙门氏菌进入培养的上皮细胞的能力严重缺陷。invF和invG的核苷酸序列表明,这些基因分别编码预测分子量为24,373和62,275的多肽。当invF和invG在基于噬菌体T7 RNA聚合酶的表达系统中表达时,观察到了相似大小的蛋白质。将InvF的预测序列与现有数据库中的翻译序列进行比较表明,该蛋白质与原核转录调节因子的AraC家族成员同源。然而,invF中的突变并未显著影响inv位点其他成员的表达。发现InvG与特殊转运蛋白的PulD家族成员同源。这种同源性表明,InvG可能是侵袭相关决定因素输出所必需的,或者参与促进进入的超分子结构的组装。

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