Disease relevance of plcA

• The beta-glucoside cellobiose has been reported to specifically repress the PrfA-dependent virulence genes hly and plcA in Listeria monocytogenes NCTC 7973 [1].

High impact information on plcA

• The system was successfully tested using the promoter of the inducible virulence gene plcA [2].
• Although plcA expression is known to depend on PrfA, a prfA promoter-lacZ fusion was highly expressed both inside and outside cells [3].
• Transcriptional hlyA and plcA fusions to luxAB were used to monitor virulent gene expression in the presence of various disaccharides [4].
• Significantly decreased transcription of the plcA gene, encoding a phospholipase C involved in vacuolar escape and cell-to-cell spread, was observed in acid-adapted bacteria [5].
• The remaining hemolytic L. monocytogenes isolates lacking the plcA gene and PI-PLC assay activity were, however, non-pathogenic via mice and chick-embryo inoculation tests, in spite of having the hlyA gene [6].

Biological context of plcA

• Increased plcA transcript levels, which were similar in both host cell vacuole and cytosol, were associated with increases in both prfA expression and PrfA activity. qRT-PCR assays were designed to measure expression of prfA from each of its three promoter regions [7].

Analytical, diagnostic and therapeutic context of plcA

• This particular strain was revealed to be avirulent and defective in hlyA and plcA in PCR amplification [8].

References