Dual roles of plcA in Listeria monocytogenes pathogenesis

Abstract

The plcA gene of Listeria monocytogenes encodes a secreted phosphatidylinositol‐speciftc phospholi‐pase C (PI‐PLC). Recent studies have established that transposon mutations within plcA result in avirulence for mice and pleiotropic effects when examined in tissue‐culture models of infection. Genetic analysis reveals that many of the effects of the transposon insertions are due to loss of readthrough transcription from plcA into the downstream gene prfA, which encodes an essential transcription factor of numerous L. monocytogenes virulence genes. Construction of an in‐frame deletion within plcA had no effect on expression of prfA thus allowing direct assignment of a role of the PI‐PLC in pathogenesis. PI‐PLC was shown to play a significant role in mediating escape of L. monocytogenes from phagosomes of primary murine macrophages. Interestingly, this defect manifested itself in vivo in the liver but not in the spleen of infected mice.