Disease relevance of ompR

• Isolation and characterization of a substitution mutation in the ompR gene of Salmonella typhimurium LT2 [1].

High impact information on ompR

• A sifA(-) mutant strain had a replication defect in macrophages, similar to that of SPI-2 and ompR(-) mutant strains [2].
• All four insertions were located in the ompR/envZ regulon [3].
• As OmpR also controls the expression of the acid-induced virulence operon ssrAB, acid shock induction of ompR was examined to gain insight into how Salmonella links virulence with survival at extreme acid pH [4].
• This evidence, combined with the finding that relaxing DNA supercoiling with novobiocin also increased ompR transcription, suggests that acid stress induces ompR by altering local DNA topology, not by changing the phosphorylation status of OmpR [4].
• The sequence data also showed that ompR and envZ form an operon, where the coding regions overlap by four base-pairs [5].

Chemical compound and disease context of ompR

• Characterization of defined ompR mutants of Salmonella typhi: ompR is involved in the regulation of Vi polysaccharide expression [6].

Biological context of ompR

• Delayed activation of programmed macrophage cell death is not observed with serotype Typhimurium strains mutated in ompR or SPI2 [7].
• The DNA sequence data were used to identify appropriate restriction sites for generating a defined deletion of 517 bp within the open reading frame of the ompR gene [6].
• The ompB operon, comprising the ompR and envZ genes, was cloned from a Salmonella typhi Ty2 cosmid bank and characterized by DNA sequence analysis [6].
• Expression of proU is independent of the ompR gene, known to be involved in osmoregulation of porin expression [8].
• An insertion mutagenesis strategy designed to reveal genes associated with acid-inducible stationary-phase acid tolerance (stationary-phase ATR) yielded two insertions in the response regulator gene ompR [9].

Anatomical context of ompR

• An equivalent to bacterial ompR genes is encoded on the plastid genome of red algae [10].

Other interactions of ompR

• The osmoinducibility of invA was independent of ompR, which controls the osmoinducibility of other genes [11].
• On the other hand, the ompR and rpoS mutations did not affect either the motility phenotype or flhD expression [12].
• Enteritidis strains from human disease, food and animals expressed the rdar morphotype at 28 degrees C. Regulation of the rdar morphotype occurred via the response regulator ompR, which activated transcription of csgD required for production of cellulose and curli fimbriae [13].
• We also provide direct evidence for the regulation of SPI-2 by the Salmonella transcription factors ompR and ssrB in vivo [14].

Analytical, diagnostic and therapeutic context of ompR

• The presence of the deletions within ompR was confirmed by Southern hybridization and sequencing of the DNA fragments surrounding the deleted regions by PCR [6].

References