Disease relevance of inlC

• By direct and inverse polymerase chain reactions (PCR), we cloned a 5.4-kb region containing a homologous gene (termed i-inlC) from L. ivanovii, the other pathogenic member of the genus Listeria [1].

High impact information on inlC

• In contrast to the transcription of the InlAB operon, which is downregulated after shift of an L. monocytogenes EGD culture from brain-heart infusion into minimum essential medium (MEM), transcription of inlC is induced in MEM like most of the other known PrfA-regulated virulence genes [2].
• In addition, InlC is strongly transcribed in the cytoplasm of phagocytic J774 cells whereas inlA is poorly transcribed under these conditions, suggesting that internalin C may play a role in a late stage of L. monocytogenes infection rather than in the uptake of L. monocytogenes by non-professional phagocytic cells [2].
• The amino acid sequence of the gene product revealed a protein of 297 amino acids that carried eight repeat units with high homology to those of the two known internalin proteins A and B. This secretory protein, termed internalin C, is much smaller than InlA or InlB and its complete sequence is related to the two known internalins [2].
• Heterologous plaque assays with L. monocytogenes-infected P388D1 macrophages as vectors demonstrate efficient spreading of L. monocytogenes into HBMEC, fibroblasts, hepatocytes, and epithelial cells, and this phenomenon is independent of the inlC gene product [3].
• Several observations implicate InlC in infection: inlC has the same transcriptional activator as other virulence genes, it is only present in pathogenic Listeria strains and an inlC deletion mutant is significantly less virulent [4].

Chemical compound and disease context of inlC

• We have recently cloned and characterized the inlC gene of Listeria monocytogenes which belongs to the listerial internalin multigene family and codes for a 30-kDa secreted protein containing five consecutive leucine-rich repeats [1].

Biological context of inlC

• Transcription of i-inlC and i-inlD is strictly dependent on the transcriptional activator PrfA, which regulates transcription of most of the known virulence genes (including inlC) of L. monocytogenes and of L. ivanovii [1].
• This chromosomal position of the two inlC genes on their respective chromosomes may be due to horizontal transfer of this gene [1].
• A putative transcriptional regulator gene, the product of which contains the TetR family signature, is located downstream of i-inlC [1].

Anatomical context of inlC

• We show that L. monocytogenes invades human umbilical vein endothelial cells independently of internalin A, internalin B, internalin C, and ActA [5].

Other interactions of inlC

• Expression of actA and plcB precedes that of inlC after infection of epithelial cells and macrophages [6].
• A subsequent gel extraction and sequence typing analysis of the highly polymorphic intragenic regions in inlB and inlC simplified a previously developed multi-virulence-locus sequence typing scheme and provided discriminatory power for subtyping L. monocytogenes similar to pulsed-field gel electrophoresis analysis [7].

References