Loh John T, Cover Timothy L
Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Infect Immun. 2006 May;74(5):3052-9. doi: 10.1128/IAI.74.5.3052-3059.2006.
In this study, we investigated a potential requirement of two-component signal transduction systems for acid resistance in Helicobacter pylori. In comparison to a wild-type strain, isogenic strains with null mutations in either HP0165 or HP1364 histidine kinases were impaired in their ability to grow at pH 5.0. The growth of complemented mutant strains was similar to that of the wild-type strain. H. pylori DNA array analyses and transcriptional reporter assays indicated that acid-responsive gene transcription was altered in the HP0165 and HP1364 null mutant strains compared to the parental wild-type strain. These results indicate that intact HP0165 and HP1364 histidine kinases are required for acid resistance in H. pylori.
在本研究中,我们调查了幽门螺杆菌中双组分信号转导系统对耐酸性的潜在需求。与野生型菌株相比,HP0165或HP1364组氨酸激酶发生无效突变的同基因菌株在pH 5.0条件下的生长能力受损。互补突变菌株的生长与野生型菌株相似。幽门螺杆菌DNA阵列分析和转录报告基因检测表明,与亲本野生型菌株相比,HP0165和HP1364无效突变菌株中酸反应性基因转录发生了改变。这些结果表明,完整的HP0165和HP1364组氨酸激酶是幽门螺杆菌耐酸性所必需的。