Shigella flexneri is an enterobacterium responsible for shigellosis, whose virulence phenotype is due to the presence of a virulence plasmid (pINV). camA (ybjX) is a gene of unknown function localized on the chromosome, and it shares homology with virK, located on the virulence plasmid. VirK protein is known to be involved in the post-transcriptional regulation of IcsA, required for intercellular spreading. Analysis of the predicted structures of CamA and VirK indicates that they share homology leading to the hypothesis that they might have a similar function in virulence. Since no data are available on the function of CamA in Shigella, we identified the camA promoter and analysed the positive role of PhoPQ in its regulation. We experimentally assessed that CamA is localized in the outer membrane. By isolating mutants lacking camA, virK or both genes we observed that the lack of either gene significantly reduces the resistance of S. flexneri to polymyxin B and that the double mutant is much more sensitive than the single mutants. We are currently defining the complementary role of the two proteins and the evolutionary significance of their presence in the Shigella genome.
Understanding the functional homology of CamA and VirK proteins in Shigella flexneri / Coluccia, M; Martorana, A.; BONACCORSI DI PATTI, Maria Carmela; Roncarati, D.; Scarlato, V.; Grossi, M.; Prosseda, G.. - (2022), pp. 104-104. (Intervento presentato al convegno XVI Congress FISV 2022 tenutosi a Portici, Italy).
Understanding the functional homology of CamA and VirK proteins in Shigella flexneri
M Coluccia;BONACCORSI DI PATTI;M. Grossi;G. Prosseda
2022
Abstract
Shigella flexneri is an enterobacterium responsible for shigellosis, whose virulence phenotype is due to the presence of a virulence plasmid (pINV). camA (ybjX) is a gene of unknown function localized on the chromosome, and it shares homology with virK, located on the virulence plasmid. VirK protein is known to be involved in the post-transcriptional regulation of IcsA, required for intercellular spreading. Analysis of the predicted structures of CamA and VirK indicates that they share homology leading to the hypothesis that they might have a similar function in virulence. Since no data are available on the function of CamA in Shigella, we identified the camA promoter and analysed the positive role of PhoPQ in its regulation. We experimentally assessed that CamA is localized in the outer membrane. By isolating mutants lacking camA, virK or both genes we observed that the lack of either gene significantly reduces the resistance of S. flexneri to polymyxin B and that the double mutant is much more sensitive than the single mutants. We are currently defining the complementary role of the two proteins and the evolutionary significance of their presence in the Shigella genome.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.