Sur7 mediates a novel pathway for PIP regulation in that promotes stress resistance and cell wall morphogenesis.

The human fungal pathogen can cause lethal systemic infections due to its ability to resist stress from the host and to undergo invasive hyphal growth. Previous studies showed that plasma membrane MCC/eisosome domains were important for virulence by promoting the ability of Sur7 to mediate normal cell wall morphogenesis and stress resistance. The mutant displayed abnormal clusters of PIP, suggesting that misregulation of this lipid underlies the phenotype. To test this, we increased PIP levels by deleting combinations of the three PIP 5' phosphatase genes (, , and ) and found that some combinations, such as , gave phenotypes similar the mutant. In contrast, deleting one copy of , the gene that encodes the 5' kinase needed to create PIP, reduced the abnormal PIP clusters and also decreased the abnormal cell wall and stress sensitive phenotypes of the mutant. Additional studies support a model that the abnormal PIP patches recruit septin proteins, which in turn promote aberrant cell wall growth. These results identify Sur7 as a novel regulator of PIP and highlight the critical role of PIP in the regulation of virulence properties.