Conserved and acquired: Decoding YbjX and VirK in the pathogenicity of Shigella flexneri
Marco Coluccia, Martina Pasqua, Davide Roncarati, Alessandra M. Martorana, Ludovica Altieri, Maria Carmela Bonaccorsi, Alessandra Polissi, Milena Grossi, Bianca Colonna, Gianni Prosseda
TL;DR
This paper explores how two proteins, YbjX and VirK, contribute to the pathogenicity of Shigella flexneri, a bacterium that causes dysentery.
Contribution
The study reveals a synergistic role of YbjX and VirK in maintaining outer membrane integrity and modulating host immune responses in Shigella.
Findings
VirK deficiency increases outer membrane permeability and host cell inflammation.
YbjX shows a complementary role when both genes are deleted.
PhoPQ regulates the expression of both ybjX and virK.
Abstract
The pathogenicity of Shigella spp. human pathogens responsible for bacillary dysentery, results from the combination of factors encoded both on the chromosome and on the virulence plasmid acquired during pathoadaptation. While many key elements have been extensively investigated, several remain poorly characterized. Among these, YbjX and VirK exhibit high structural similarity and are encoded by genes located on the chromosome and the virulence plasmid, respectively. We provide a molecular and functional characterization of Shigella flexneri YbjX and VirK. We defined the ybjX and virK promoter regions and confirmed that their expression is regulated by the PhoPQ two-component system. Localization studies demonstrated that both proteins are cytoplasmic. In silico analysis predicted a similar structure for the two proteins, resembling members of the Gcn5-related N-acetyltransferase…
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Taxonomy
TopicsEscherichia coli research studies · Viral gastroenteritis research and epidemiology · Salmonella and Campylobacter epidemiology