Sandbox Reserved 1659: Difference between revisions
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== | == Function == | ||
Once the bacteria reaches the host's cytoplasm, the expression of LntA is activated, the protein is excreted and addressed to the nucleus thanks to a peptide signal. Then, LntA interacts with the transcription factor BAHD1 (link to a presentation and the structure of BAHD1). In absence of infection, BAHD1 represses the expression of ISG by promoting the local formation of heterochromatin while the interaction of LntA with BAHD1 has the effect of removing the chromatin repressor from the host’s DNA. Therefore, L. monocytogenes virulence factor induces a strong interferon response which enhances its pathogenicity. | Once the bacteria reaches the host's cytoplasm, the expression of LntA is activated, the protein is excreted and addressed to the nucleus thanks to a peptide signal. Then, LntA interacts with the transcription factor BAHD1 (link to a presentation and the structure of BAHD1). In absence of infection, BAHD1 represses the expression of ISG by promoting the local formation of heterochromatin while the interaction of LntA with BAHD1 has the effect of removing the chromatin repressor from the host’s DNA. Therefore, L. monocytogenes virulence factor induces a strong interferon response which enhances its pathogenicity. | ||
The mechanisms by which Listeria benefits from the synthesis of interferons are not fully understood. One hypothesis could be that Listeria monocytogenes takes advantage of the arrest of cellular-cycle induced by interferons (6). Indeed, this mechanism could be similar to those used by other pathogens such as Salmonella (7) or Yersinia (8) which are able to promote an inflammatory response in gut epithelium in order to facilitate their dissemination and colonization. | The mechanisms by which Listeria benefits from the synthesis of interferons are not fully understood. One hypothesis could be that Listeria monocytogenes takes advantage of the arrest of cellular-cycle induced by interferons (6). Indeed, this mechanism could be similar to those used by other pathogens such as Salmonella (7) or Yersinia (8) which are able to promote an inflammatory response in gut epithelium in order to facilitate their dissemination and colonization. | ||
