Candida albicans is a human commensal microorganism that can cause life-threatening systemic infections in immunocompromised individuals. A significant virulence trait of C. albicans is its ability to undergo transition between yeast and hyphal (filamentous) morphologies. The hyphal switch allows effective invasion of host tissues, and confers the ability to form biofilms and to block an adaptive immune response. To date, there is a shortage in effective treatments of candidiasis. Thus the suppression of hyphal morphogenesis is of both fundamental and therapeutic importance.
In a screen for kinases able to suppress hyphal morphogenesis, we identified Akl1, whose homolog in baker’s yeast is involved in the regulation of endocytosis. We find that CaAKL1 overexpression suppresses hyphal morphogenesis, whereas deletion of this gene leads to a more filamentous morphology. CaAKL1 overexpression suppressed fluid phase endocytosis while its knockout strain exhibited higher levels of endocytosis. Interestingly, CaAKL1 deletion was found to enhance endocytosis at the hyphal-inducing temperature of 37°C but not at 30°C. This was true even in the hyphal morphogenesis-deficient Caume6-/- background, suggesting that the effect of CaAkl1 on morphogenesis is an indirect consequence of its effect on endocytosis, rather than the other way round. These results highlight the importance of the little-studied role of endocytosis in hyphal morphogenesis.
