hilA is a novel ompR/toxR family member that activates the expression of Salmonella typhimurium invasion genes

hilA is a novel ompR/toxR family member that activates the expression of Salmonella typhimurium invasion genes
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DOI:
10.1111/j.1365-2958.1995.mmi_18040715.x
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发表时间:
1995-11-01
影响因子:
3.6
通讯作者:
Lee, CA
Lee, CA
中科院分区:
生物学2区
文献类型:
--
作者:
Bajaj, V;Hwang, C;Lee, CA

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在感染宿主期间,沙门氏菌进入肠上皮细胞。细菌进入宿主细胞所需的许多鼠伤寒沙门氏菌基因均在 40 kb 的“致病岛”上编码。我们在这里报告了 hilA 的鉴定,它是“岛”内的一个基因,似乎编码入侵基因表达的激活剂。通过使用一组与鼠伤寒沙门氏菌入侵基因的lacZY转录融合,我们发现hilA激活位于“致病岛”上的入侵基因的表达。 hilA 是体外有效进入 HEp-2 细胞所必需的。预测的 hilA 氨基酸序列与转录激活因子 OmpR-ToxR 家族的 DNA 结合结构域具有显着的同源性。然而,与 OmpR 和 ToxR 不同,HilA 既不包含磷酰基受体也不包含跨膜结构域,因此,其活性可能受到新机制的调节。许多环境条件调节沙门氏菌进入非吞噬哺乳动物细胞的能力。有人提出,沙门氏菌入侵蛋白的诱导响应环境因素的组合,确保细菌进入仅限于感染期间的特定部位和时间。我们的结果与 hilA 在感染过程中沙门氏菌入侵调节中发挥关键作用的假设是一致的。
During infection of its hosts, Salmonella enters intestinal epithelial cells. Many Salmonella typhimurium genes required for bacterial entry into host cells are encoded on a 40 kb 'pathogenicity island'. We report here the identification of hilA, a gene within the 'island' that appears to encode an activator of invasion gene expression. By using a set of lacZY transcriptional fusions to S. typhimurium invasion genes, we found that hilA activates the expression of invasion genes located on the 'pathogenicity island'. hilA is required for efficient entry into HEp-2 cells in vitro. The predicted amino acid sequence of hilA shares significant homology with the DNA-binding domains of the OmpR-ToxR family of transcriptional activators. However, unlike OmpR and ToxR, HilA contains neither a phosphoryl acceptor nor a membrane-spanning domain, and, therefore, its activity may be modulated by a novel mechanism. Many environmental conditions modulate the ability of Salmonella to enter non-phagocytic mammalian cells. It has been proposed that induction of Salmonella invasion proteins in response to a combination of environmental cues ensures that bacterial entry is limited to specific sites and times during infection. Our results are consistent with the hypothesis that hilA plays a key role in the regulation of Salmonella invasion during infection.