Candida albicans undergoes a dramatic morphological transition in response
to various growth conditions. This ability to switch from a yeast form to a
hyphal form is required for its pathogenicity. The intractability of Candi
da to traditional genetic approaches has hampered the study of the molecula
r mechanism governing this developmental switch. Our approach is to use the
more genetically tractable yeast Saccharomyces cerevisiae to yield clues a
bout the molecular control of filamentation for further studies in Candina.
G(1) cyclins Cln1 and Cln2 have been implicated in the control of morphoge
nesis in S. cerevisiae. We show that C. albicans CLN1 (CaCLN1) has the same
cell cycle-specific expression pattern as CLN1 and CLN2 of S. cerevisiae.
To investigate whether G(1) cyclins are similarly involved in the regulatio
n of cell morphogenesis during the yeast-to-hypha transition of C. albicans
, we mutated CaCLN1. Cacln1/Cacln1 cells were found to be slower than wild-
type cells in cell cycle progression. The Cacln1/Cacln1 mutants were also d
efective in hyphal colony formation on several solid media. Furthermore, wh
ile mutant strains developed germ tubes under several hypha-inducing condit
ions, they were unable to maintain the hyphal growth mode in a synthetic hy
pha-inducing liquid medium and were deficient in the expression of hypha-sp
ecific genes in this medium. Our results suggest that CaCln1 may coordinate
ly regulate hyphal development with signal transduction pathways in respons
e to various environmental cues.