A plant MinD homologue rescues <it>Escherichia coli </it>HL1 mutant (Δ<it>MinDE</it>) in the absence of MinE
2009
Gao Hongbo | Jia Jingjing | Hu Yong | Zhang Min | He Yikun
<p>Abstract</p> <p>Background</p> <p>In <it>E. coli</it>, the Min operon (<it>MinCDE</it>) plays a key role in determining the site of cell division. MinE oscillates from the middle to one pole or another to drive the MinCD complex to the end of the cell. The MinCD complex prevents FtsZ ring formation and the subsequent cell division at cell ends. In <it>Arabidopsis thaliana</it>, a homologue of MinD has been shown to be involved in the positioning of chloroplast division site.</p> <p>Results</p> <p>To learn whether the MinD homologue in plants is functional in bacteria, AtMinD was expressed in <it>E. coli</it>. Surprisingly, AtMinD can rescue the minicell phenotype of <it>E. coli </it>HL1 mutant (Δ<it>MinDE</it>) in the absence of EcMinE. This rescue requires EcMinC. AtMinD was localized to puncta at the poles of <it>E. coli </it>cells and puncta in chloroplasts without oscillation. AtMinD expressed in the HL1 mutant can cause a punctate localization pattern of GFP-EcMinC at cell ends. Yeast two hybrid and BiFC analysis showed that AtMinD can interact with EcMinC.</p> <p>Conclusion</p> <p>Similar to the MinD in <it>Bacillus subtilis</it>, AtMinD is localized to the polar region in <it>E. coli </it>and interacts with EcMinC to confine EcFtsZ polymerization and cell division at the midpoint of the cell.</p>
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