Disease relevance of invF

• The Salmonella typhimurium invasion genes invF and invG encode homologues of the AraC and PulD family of proteins [1].
• Proteins of similar sizes were observed when invF and invG were expressed in a bacteriophage T7 RNA polymerase-based expression system [1].
• The introduction of plasmids encoding invF and sicA into a non-pathogenic E. coli K-12 strain stimulated the transcription of both a sicA- and a sigD-lacZYA promoter fusion [2].

High impact information on invF

• The DeltarelADeltaspoT strain exhibited severely reduced expression of hilA and invF, encoding major transcriptional activators required for Salmonella pathogenicity island 1 (SPI-1) gene expression and at least two other pathogenicity islands [3].
• This decreased expression of hilA and invF resulted in an altered secreted invasion protein profile in the fis mutant [4].
• In order to understand how HilA controls the transcription of SPI-1 genes, we have analysed the invF and prgH promoters [5].
• This excessive induction of apoptosis was abrogated by disruption of invF, which is required for the expression of the Salmonella pathogenicity island 1 (SPI1) genes [6].
• Transcription assays demonstrated that invasion gene regulators (e.g., sirC and invF) are repressed by bile [7].

Biological context of invF

• However, neither SirA nor HilA is believed to directly activate the promoters of these genes. invF, the first gene of the inv-spa gene cluster, is predicted to encode an AraC-type transcriptional activator and is required for invasion into cultured epithelial cells [8].
• The nucleotide sequences of invF and invG indicated that these genes encode polypeptides with predicted molecular weights of 24,373 and 62,275, respectively [1].

Other interactions of invF

• Genetic evidence is also presented suggesting there is HilA-dependent readthrough transcription from the invF promoter at least through sipC [8].

References