Reference: Zhou Z, et al. (2002) [Cloning of Candida albicans CaBEM1 and its role in filamentous growth of Saccharomyces cerevisiae]. Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 34(5):553-9

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Abstract


The pathogenic fungus Candida albicans has a dimorphic transition in various environmental conditions. Many regulatory factors and several transduction pathways have been identified in controlling filamentous growth. G(1) cyclins Cln1 and Cln2 have been reported as involved in the control of morphogenesis in Saccharomyces cerevisiae. Diploid cln1/cln1 and cln2/cln2 strains completely lost the ability to form pseudohyphae. A C. albicans genomic DNA library was introduced into cln1/cln1 and cln2/cln2 mutants to screen genes which could complement its filamentous growth defect. In this screening a BEM1 homolog, CaBEM1, was identified. The CaBEM1 gene has an ORF of 1 899 bp, encoding a putative protein of 632 amino acids. The CaBem1 protein shares highest homology in amino acids with Bem1 (38%) of S. cerevisiae and Scd2 (32%) of Schizosaccharomyces pombe. Sequence analysis showed that the CaBem1 contains two N-terminal SH3 domains, a PX domain and a C-terminal PB1 domain. It is believed these domains are required for binding to proteins involved in polarized growth in S. cerevisiae and S. pombe. Ectopic expression of the CaBEM1 gene in diploid S. cerevisiae suppressed defects in filamentous growth of some mutants under nitrogen starvation conditions. This suppression bypassed MAPK pathway and cAMP/PKA pathway in filamentous growth. These results suggest that the CaBem1 protein may be a downstream component of these two signal transduction pathways of filament formation.

Reference Type
Journal Article | Research Support, Non-U.S. Gov't
Authors
Zhou Z, Liu HP, Chen JY
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