TUP1, CPH1 and EFG1 make independent contributions to filamentation in candida albicans.
نویسندگان
چکیده
The common fungal pathogen, Candida albicans, can grow either as single cells or as filaments (hyphae), depending on environmental conditions. Several transcriptional regulators have been identified as having key roles in controlling filamentous growth, including the products of the TUP1, CPH1, and EFG1 genes. We show, through a set of single, double, and triple mutants, that these genes act in an additive fashion to control filamentous growth, suggesting that each gene represents a separate pathway of control. We also show that environmentally induced filamentous growth can occur even in the absence of all three of these genes, providing evidence for a fourth regulatory pathway. Expression of a collection of structural genes associated with filamentous growth, including HYR1, ECE1, HWP1, ALS1, and CHS2, was monitored in strains lacking each combination of TUP1, EFG1, and CPH1. Different patterns of expression were observed among these target genes, supporting the hypothesis that these three regulatory proteins engage in a network of individual connections to downstream genes and arguing against a model whereby the target genes are regulated through a central filamentous growth pathway. The results suggest the existence of several distinct types of filamentous forms of C. albicans, each dependent on a particular set of environmental conditions and each expressing a unique set of surface proteins.
منابع مشابه
Chlamydospore formation in Candida albicans requires the Efg1p morphogenetic regulator.
Chlamydospore formation of the fungal pathogen Candida albicans was found to depend on the Efg1 protein, which regulates the yeast-hyphal transition. Isogenic mutants lacking EFG1 or encoding T206A and T206E variants did not differentiate chlamydospores, while cek1, cph1, or tpk2 mutations had no effect. Furthermore, filamentation of efg1 cph1 double mutants in microaerophilic conditions sugges...
متن کاملN-Acetylglucosamine Kinase, HXK1 Is Involved in Morphogenetic Transition and Metabolic Gene Expression in Candida albicans
Candida albicans, a common fungal pathogen which diverged from the baker's yeast Saccharomyces cerevisiae has the unique ability to utilise N-acetylglucosamine, an amino sugar and exhibits phenotypic differences. It has acquired intricate regulatory mechanisms at different levels in accordance with its life style. N-acetylglucosamine kinase, a component of the N-acetylglucosamine catabolic casc...
متن کاملCrk1, a novel Cdc2-related protein kinase, is required for hyphal development and virulence in Candida albicans.
Both mitogen-activated protein kinases and cyclin-dependent kinases play a role in hyphal development in Candida albicans. Using an oligonucleotide probe-based screen, we have isolated a new member of the Cdc2 kinase subfamily, designated Crk1 (Cdc2-related kinase). The protein sequence of Crk1 is most similar to those of Saccharomyces cerevisiae Sgv1 and human Pkl1/Cdk9. In S. cerevisiae, CRK1...
متن کاملNon-lethal Candida albicans cph1/cph1 efg1/efg1 mutant partially protects mice from systemic infections by lethal wild-type cells.
Although Candida albicans cph1/cph1 efg1/efg1 mutant cells are not lethal to mice, they proliferated in infected mice instead of simply being cleared by the host immune system. Here, we have shown that the cph1/cph1 efg1/efg1 mutant partially protects mice from systemic infections by the lethal wild-type Candida albicans cells. Our results further indicate that a second dose of the cph1/cph1 ef...
متن کاملCandida albicans morphologies revealed by scanning electron microscopy analysis
Scanning electron microscope (SEM) observations were used to analyze particular morphologies of Candida albicans clinical isolate (strain 82) and mutants defective in hyphae-promoting genes EFG1 (strain HLC52) and/or CPH1 (strains HLC54 and Can16). Transcription factors Efg1 and Cph1 play role in regulating filamentation and adhesion of C. albicans' morphologies. Comparative analysis of such mu...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Genetics
دوره 155 1 شماره
صفحات -
تاریخ انتشار 2000