Role of LrrkA in the Control of Phagocytosis and Cell Motility in .

LrrkA is a kinase with leucine-rich repeats. LrrkA stimulates Kil2 and intra-phagosomal killing of ingested bacteria in response to folate. In this study, we show that genetic inactivation of also causes a previously unnoticed phenotype: KO cells exhibit enhanced phagocytosis and cell motility compared to parental cells. This phenotype is cell autonomous, is reversible upon re-expression of LrrkA, and is not due to an abnormal response to inhibitory quorum-sensing factors secreted by in its medium. In addition, folate increases motility in parental cells, but not in KO cells, suggesting that LrrkA plays a pivotal role in the cellular response to folate. On the contrary, KO cells regulate gene transcription in response to folate in a manner indistinguishable from parental cells. Overall, based on analysis of mutant phenotypes, we identify gene products that participate in the control of intracellular killing, cell motility, and gene transcription in response to folate. These observations reveal a mechanism by which encountering bacterially-secreted folate can migrate, engulf, and kill bacteria more efficiently.