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通过分离温度调节型inv::lacZ操纵子融合体鉴定志贺氏菌侵袭基因。

Identification of Shigella invasion genes by isolation of temperature-regulated inv::lacZ operon fusions.

作者信息

Hromockyj A E, Maurelli A T

机构信息

Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.

出版信息

Infect Immun. 1989 Oct;57(10):2963-70. doi: 10.1128/iai.57.10.2963-2970.1989.

Abstract

Penetration and multiplication within cells of the human colonic epithelium are hallmarks of Shigella spp. pathogenicity. Shigella spp. virulence is regulated by growth temperature. Strains phenotypically virulent when grown at 37 degrees C are phenotypically avirulent when grown at 30 degrees C. The number of genes involved in Shigella spp. pathogenicity and how many virulence genes are temperature regulated are unknown. To facilitate the study of temperature-regulated virulence in Shigella spp., we employed lacZ operon fusion technology to identify temperature-regulated invasion (inv) genes. Four inv::lacZ fusion mutants were identified and found to be unable to invade HeLa cells. The fusions were located in a region of the 220-kilobase invasion plasmid defined as the minimal amount of DNA required for invasion, and they were controlled by virR, the temperature-dependent virulence gene regulator. Western blot (immunoblot) and Southern hybridization analyses indicated that one of the fusions was located in a known inv gene, ipaB, which encodes one of the major immunogenic peptides of Shigella spp. This ipaB::lacZ operon fusion mutant synthesized a truncated IpaB protein recognized by IpaB-specific monoclonal antibodies. Three of the fusions were within novel genes mapping to regions previously identified as essential for a positive virulence phenotype. Analysis of bacterial surface proteins suggested that the genes marked by these fusions may play a role in the correct surface expression of the ipaB and ipaC gene products.

摘要

在人结肠上皮细胞内的穿透和增殖是志贺氏菌属致病性的标志。志贺氏菌属的毒力受生长温度调节。在37℃生长时表型有毒力的菌株在30℃生长时表型无毒力。参与志贺氏菌属致病性的基因数量以及有多少毒力基因受温度调节尚不清楚。为便于研究志贺氏菌属中温度调节的毒力,我们采用lacZ操纵子融合技术来鉴定温度调节的侵袭(inv)基因。鉴定出四个inv::lacZ融合突变体,发现它们无法侵袭HeLa细胞。这些融合位于220千碱基侵袭质粒的一个区域,该区域被定义为侵袭所需的最小DNA量,并且它们受virR调控,virR是温度依赖性毒力基因调节因子。蛋白质免疫印迹(免疫印迹)和Southern杂交分析表明,其中一个融合位于一个已知的inv基因ipaB中,该基因编码志贺氏菌属的主要免疫原性肽之一。这个ipaB::lacZ操纵子融合突变体合成了一种被IpaB特异性单克隆抗体识别的截短IpaB蛋白。其中三个融合位于新基因内,这些新基因定位于先前确定对阳性毒力表型至关重要的区域。对细菌表面蛋白的分析表明,这些融合所标记的基因可能在ipaB和ipaC基因产物的正确表面表达中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c04c/260756/3da8844433a9/iai00070-0050-a.jpg

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