RT Journal Article
SR Electronic
T1 The G<sub>1</sub> Cyclin Cln3 Regulates Morphogenesis in <em>Candida albicans</em>
JF Eukaryotic Cell
JO Eukaryot Cell
FD American Society for Microbiology
SP 90
OP 94
DO 10.1128/EC.4.1.90-94.2005
VO 4
IS 1
A1 Chapa y Lazo, Bernardo
A1 Bates, Steven
A1 Sudbery, Peter
YR 2005
UL http://ec.asm.org/content/4/1/90.abstract
AB In Saccharomyces cerevisiae, the G1 cyclin Cln3 initiates the Start of a mitotic cell cycle in response to size and nutrient inputs. Loss of Cln3 delays but does not prevent Start, due to the eventual Cln3-independent transcription of CLN1 and CLN2. When unbudded cells of the human pathogen Candida albicans were depleted of the G1 cyclin Cln3 they increased in size but did not bud. Thus, unlike S. cerevisiae, Cln3 is essential for budding in C. albicans. However, eventually the large unbudded cells spontaneously produced filamentous forms. The morphology was growth medium dependent; on nutritionally poor medium the polarized outgrowths fulfilled the formal criteria for true hyphae. This state is stable, and continued growth leads to a hyphal mycelium, which invades the agar substratum. Interestingly, it is also required for normal hyphal development, as Cln3-depleted cells develop morphological abnormalities if challenged with hyphal inducing signals such as serum or neutral pH. Taken together, these results show that, in C. albicans, Cln3 has assumed a critical role in coordinating mitotic cell division with differentiation.