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Sphingolipids are involved in several cellular functions, including maintenance of cell wall integrity. To gain insight into the role of individual genes of sphingolipid biosynthetic pathway, we have screened  Saccharomyces cerevisiae  strains deleted in these genes for sensitivity to cell wall perturbing agents calcofluor white and congo red. Only deletants of  FEN1  and  SUR4  genes were found to be sensitive to both these agents.  Candida albicans  strains deleted in their orthologs,  CaFEN1  and  CaFEN12,  respectively, also showed comparable phenotypes, and a strain deleted for both these genes was extremely sensitive to cell wall perturbing agents. Deletion of these genes was reported earlier to sensitise cells to amphotericin B (AmB), which is a polyene drug that kills the cells mainly by binding and sequestering ergosterol from the plasma membrane. Here we show that their AmB sensitivity is likely due to their cell wall defect. Further, we show that double deletant of  C. albicans  is defective in hyphae formation as well as biofilm development. Together this study reveals that deletion of  FEN1  and  SUR4  orthologs of  C. albicans  leads to impaired cell wall integrity and biofilm formation, which in turn sensitise cells to AmB.

Critical role for CaFEN1 and CaFEN12 of Candida albicans in cell wall integrity and biofilm formation