Sandbox Reserved 1659: Difference between revisions
From Proteopedia
Jump to navigationJump to search
No edit summary |
No edit summary |
||
| Line 8: | Line 8: | ||
== Function == | == 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. | ||
In addition, Lebreton et al showed that when listeria grows outside the cell, the transcription rate of lntA is almost null and that a constitutive expression of LntA has an antibacterial effect. Thus, the efficiency of LntA requires a precise temporal and quantitative regulation. | In addition, Lebreton et al showed that when listeria grows outside the cell, the transcription rate of lntA is almost null and that a constitutive expression of LntA has an antibacterial effect. Thus, the efficiency of LntA requires a precise temporal and quantitative regulation. | ||
| Line 26: | Line 26: | ||
== References == | == References == | ||
<references/> | <references/> | ||
Lebreton A, Job V, Ragon M, Le Monnier A, Dessen A, Cossart P, Bierne H. 2014. Structural basis for the inhibition of the chromatin repressor BAHD1 by the | |||
bacterial nucleomodulin LntA. | |||
Alice Lebreton. Régulations post-transcriptionnelles de l’expression génique de la cellule hôte en réponse à l’infection bactérienne. Sciences du Vivant, 2015. | |||
Lebreton A, Cossart P, Bierne H. Bacteria tune interferon responses by playing with chromatin. Virulence. 2012 | |||
Dussurget O, Bierne H, Cossart P. The bacterial pathogen Listeria monocytogenes and the interferon family: type I, type II and type III interferons. Front Cell Infect Microbiol. 2014 | |||
Lebreton A, Lakisic G, Job V, Fritsch L, Tham TN, Camejo A, Matteï PJ, Regnault B, Nahori MA, Cabanes D, Gautreau A, Ait-Si-Ali S, Dessen A, Cossart P, Bierne H. A bacterial protein targets the BAHD1 chromatin complex to stimulate type III interferon response. Science. 2011 https://science.sciencemag.org/content/331/6022/1271 | |||
ROHDE JOHN R. Listeria unwinds host’s DNA. SCIENCE, 2011 : 1271-1272 | |||
Winter SE, Thiennimitr P et al. Gut inflammation provides a respiratory electron acceptor for Salmonella. Nature. 2010 | |||
Dewoody, R., Merritt, P.M., Houppert, A.S. and Marketon, M.M. (2011), YopK regulates the Yersinia pestis type III secretion system from within host cells. Molecular Microbiology, 79: 1445-1461. https://doi.org/10.1111/j.1365-2958.2011.07534.x | |||
