Maintenance of the cell morphology by MinC in Helicobacter pylori
Pei-Yu Chiou1, Cheng-Hung Luo, Kai-Chih Chang
1Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Abstract:
In the model organism Escherichia coli, Min proteins are involved in regulating the division of septa formation. The computational genome analysis of Helicobacter pylori, a gram-negative microaerophilic bacterium causing gastritis and peptic ulceration, also identified MinC, MinD, and MinE. However, MinC (HP1053) shares a low identity with those of other bacteria and its function in H. pylori remains unclear. In this study, we used morphological and genetic approaches to examine the molecular role of MinC. The results were shown that an H. pylori mutant lacking MinC forms filamentous cells, while the wild-type strain retains the shape of short rods. In addition, a minC mutant regains the short rods when complemented with an intact minCHp gene. The overexpression of MinCHp in E. coli did not affect the growth and cell morphology. Immunofluorescence microscopy revealed that MinCHp forms helix-form structures in H. pylori, whereas MinCHp localizes at cell poles and pole of new daughter cell in E. coli. In addition, co-immunoprecipitation showed MinC can interact with MinD but not with FtsZ during mid-exponential stage of H. pylori. Altogether, our results show that MinCHp plays a key role in maintaining proper cell morphology and its function differs from those of MinCEc.
Insights
The Helicobacter pylori MinC protein is crucial for maintaining bacterial cell shape, unlike its counterpart in E. coli. This study reveals MinC
Area of Science:
- Microbiology
- Cell Biology
- Bacterial Genetics
Background:
- Min proteins regulate cell division in model organisms like Escherichia coli.
- Helicobacter pylori, a bacterium causing gastritis, possesses MinC, MinD, and MinE proteins.
- The specific function of H. pylori MinC (HP1053) is unknown due to low sequence identity with other bacterial MinC proteins.
Purpose of the Study:
- To investigate the molecular role of MinC in Helicobacter pylori.
- To understand the function of MinC in bacterial cell morphology and division.
Main Methods:
- Morphological analysis of H. pylori wild-type and minC mutant strains.
- Genetic complementation of the minC mutant.
- Overexpression of H. pylori MinC (MinCHp) in E. coli.
- Immunofluorescence microscopy to determine MinCHp localization in both species.
- Co-immunoprecipitation assays to identify protein interactions.
Main Results:
- H. pylori lacking MinC exhibited filamentous cell morphology, while the wild-type showed normal short rods.
- Complementation of the minC mutant with an intact gene restored the short rod shape.
- Overexpression of MinCHp in E. coli did not alter growth or cell morphology.
- MinCHp localized in helix-form structures in H. pylori but at cell poles in E. coli.
- H. pylori MinC interacted with MinD but not FtsZ during the mid-exponential growth phase.
Conclusions:
- MinCHp plays a critical role in maintaining the proper cell morphology of Helicobacter pylori.
- The function and localization of MinCHp in H. pylori differ significantly from MinC in E. coli.
- MinCHp's interaction with MinD suggests a conserved but distinct mechanism in cell division regulation.
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