Beschreibung:
<jats:title>Abstract</jats:title>
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<jats:title>Background</jats:title>
<jats:p>The chlamydiae alter many aspects of host cell biology, including the division process, but the molecular biology of these alterations remains poorly characterized. Chlamydial inclusion membrane proteins (Incs) are likely candidates for direct interactions with host cell cytosolic proteins, as they are secreted to the inclusion membrane and exposed to the cytosol. The <jats:italic>inc</jats:italic> gene <jats:italic>CT223</jats:italic> is one of a sequential set of orfs that encode or are predicted to encode Inc proteins. CT223p is localized to the inclusion membrane in all tested <jats:italic>C. trachomatis</jats:italic> serovars.</jats:p>
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<jats:title>Results</jats:title>
<jats:p>A plasmid transfection approach was used to examine the function of the product of <jats:italic>CT223</jats:italic> and other Inc proteins within uninfected mammalian cells. Fluorescence microscopy was used to demonstrate that <jats:italic>CT223</jats:italic>, and, to a lesser extent, adjacent <jats:italic>inc</jats:italic> genes, are capable of blocking host cell cytokinesis and facilitating centromere supranumeracy defects seen by others in chlamydiae-infected cells. Both phenotypes were associated with transfection of plasmids encoding the carboxy-terminal tail of CT223p, a region of the protein that is likely exposed to the cytosol in infected cells.</jats:p>
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<jats:title>Conclusion</jats:title>
<jats:p>These studies suggest that certain Inc proteins block cytokinesis in <jats:italic>C. trachomatis</jats:italic>-infected cells. These results are consistent with the work of others showing chlamydial inhibition of host cell cytokinesis.</jats:p>
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