PMID:21896677
| Citation |
Koli, P, Sudan, S, Fitzgerald, D, Adhya, S and Kar, S (2011) Conversion of commensal Escherichia coli K-12 to an invasive form via expression of a mutant histone-like protein. MBio 2 |
|---|---|
| Abstract |
The HUα(E38K, V42L) mutant of the bacterial histone-like protein HU causes a major change in the transcription profile of the commensal organism Escherichia coli K-12 (Kar S, Edgar R, Adhya S, Proc. Natl. Acad. Sci. U. S. A. 102:16397-16402, 2005). Among the upregulated genes are several related to pathogenic interactions with mammalian cells, as evidenced by the expression of curli fibers, Ivy, and hemolysin E. When E. coli K-12/ HUα(E38K, V42L) was added to Int-407 cells, there was host cell invasion, phagosomal disruption, and intracellular replication. The invasive trait was also retained in a murine ileal loop model and intestinal explant assays. In addition to invasion, the internalized bacteria caused a novel subversion of host cell apoptosis through modification and regulation of the BH3-only proteins Bim(EL) and Puma. Changes in the transcription profile were attributed to positive supercoiling of DNA leading to the altered availability of relevant promoters. Using the E. coli K-12/HUα(E38K, V42L) variant as a model, we propose that traditional commensal E. coli can adopt an invasive lifestyle through reprogramming its cellular transcription, without gross genetic changes. |
| Links |
PubMed PMC3172693 Online version:10.1128/mBio.00182-11 |
| Keywords |
Animals; Apoptosis; Cell Line; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; Disease Models, Animal; Epithelial Cells/microbiology; Escherichia coli Infections/microbiology; Escherichia coli Infections/pathology; Escherichia coli K12/genetics; Escherichia coli K12/pathogenicity; Escherichia coli Proteins/genetics; Escherichia coli Proteins/metabolism; Female; Gene Expression; Humans; Ileum/microbiology; Mice; Mice, Inbred BALB C; Mutation, Missense; Virulence |
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