Figure 12.

Proposed model of PvrA mediated regulatory pathways. During infection, PC is degraded by lipases and PlcH, resulting in glycerol, choline and fatty acids. Glycine betaine (GB) and dimethylglycine (DMG) derived from choline are sensed by GbdR, which directly upregulates plcH (57–59). The fatty acids were converted into fatty acyl-CoA. PvrA binds to the fatty acyl-CoA and activates the expression of plcH, fadD1, fadD6, PA0508, aprA, maeB, and glcB. FadD1, FadD6 and PA0508 are key enzymes in the β-oxidation pathway through which a long-chain acyl-CoA molecule is broken down to acetyl-CoA molecules. The las quorum sensing system regulates the expression of aprA (76,77). AprA degrades self flagellin and host complement component C2 to evade recognition by the immune system (50,51). MaeB and GlcB are key enzymes in the glyoxylate shunt which plays an important role in utilizing fatty acids in bacteria (61).