Novel Na+/H+ antiporter (NapA) regulates the motility in Helicobacter pylori
1 Department of Bacteriology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
2 Department of Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
3 Department of Molecular Bacteriology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
4 Department of Biochemistry, Chiba University Graduate School of Pharmaceutical Sciences, Chiba, Japan.
Research Article
GSC Advanced Research and Reviews, 2021, 08(03), 027–035.
Article DOI: 10.30574/gscarr.2021.8.3.0188
Publication history:
Received on 28 July 2021; revised on 03 September 2021; accepted on 05 September 2021
Abstract:
Na+/H+ antiporter plays an important role in maintaining cellular homeostasis by regulating osmotic pressure and intracellular pH. It plays an important role in maintaining cellular homeostasis. In Helicobacter pylori, whole genome sequencing has revealed the presence of two types of Na+/H+ antiporter. A gene (nhaA) homologous to the Na+/H+ antiporter of Escherichia coli has been investigated and its function has been analyzed. However, another gene homologous to the Na+/H+ antiporter of Enterococcus hirae (napA) is not yet known in detail. In this study, we investigated the function of this gene (napA in H. pylori). First, to confirm the genetic presence of napA in 20 H. pylori clinical isolates, PCR analysis was performed, and the napA gene was confirmed in all strains. The amount of Na+ extrusion was measured by atomic absorption spectroscopy. The results showed that the Na+ concentration was decreased in the wild-type strain compared to the napA mutant strain. In addition, there was a significant dose-dependent difference in CFU of Na+ concentration in the napA mutant strain compared to the wild-type strain. We examined whether the napA gene is related to motility using both wild-type and napA mutant strains. As a result, in the motility agar test, the bacterial motility observed in the wild-type strain was not observed in the napA mutant strain. However, no difference in flagellar proteins was observed by SDS-PAGE analysis. These results suggest that the napA gene of H. pylori may regulate homeostasis by extruding Na+ and may also regulate motility.
Keywords:
Helicobacter pylori; NapA; Na+/H+ antiporter; Motility; Flagella
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