(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) > cellular organisms: NE > Eukaryota: NE > Opisthokonta: NE > Fungi: NE > Dikarya: NE > Ascomycota: NE > saccharomyceta: NE > Saccharomycotina: NE > Saccharomycetes: NE > Saccharomycetales: NE > Debaryomycetaceae: NE > Candida/Lodderomyces clade: NE > Candida [Debaryomycetaceae]: NE > Candida albicans: NE > Candida albicans SC5314: NE
LegendThis sequence has been compared to family alignement (MSA) red => minority aminoacid blue => majority aminoacid color intensity => conservation rate title => sequence position(MSA position)aminoacid rate Catalytic site Catalytic site in the MSA MFTHKRVPQHEEYELVNQVPPTQSPTDSPTRSESDFRNSTDSQLSDIFED LENYSGSSGQKIEDFNDSPLFQSVLMRYKNEGISGRTCGIFSLVAIFLWI GSVIIYSRVNHSTIGNDLTWKTNIIQLNGENITLNEYNPNFKNITMNDWR KGKYHTFEKQIRWLTSKQSPKSKHGGGFYVLDEHDKIVVNQIGQVDKSDT FLSNKQFEYGNNFFKIQDFILNPSQSIEDSEVVHIIITDTVHQWRHSSFA LYWLFKPLVGTYTPIQPPRNNNKGNGLEVDALDKLHYADFSSDGKYIVFG FEHNLFIQDLATGEIQQITDDGSPNIINGKSDWIYEEEVIASNKMIWWSP SGNHFIFAKINETKVQEVDMDYYTKQNTNIGMQYQQVGESKYEGVNQYPI NTQLKYPKPGTSNPILSLYIYDIANKKTEEIIDGDDNLGTEYILYYAKWI DANSFLMKQSDRTSSVLTKKLYDLDKNHVSIVSSSNVTKEYKGWVERMNP ITLLDDGKYIDNVVIDNRNTLALFDSPHSVSPSKVLVDNKDWDITGEAIY DAQEKFVYFLSTVRSSMDAHLVGIDLADNYKLYNITDTKKDGIFETKFSE NGQYLSLVYQGPNQPWQRLINMANVHDFIKSEEYGKSTIEEAVILNQPIV NSLANLKEINLPTVRYKEVTIGKKEDQVTLNIMEILPPNFKAKNQKYPLF VYTYGGPGSQTVMKKFDIGFLQIVSARLNSIILVIDPRGTGGKGWKFESF AKNNIGYWESRDLKTITSEYIKKNKKLIDKERVALWGWSYGGFVTLKTLE YDKGEVFKYGMAVAPVTNWLFYDSIYTERYMGLPDTDPNYETSARINDFD NFKSVKRFLLVHGTGDDNVHVQNLMWLLDQLNIHNVENYDMHLFPDSDHS ISYDNAGVIVYDKLYYWLQNAFRGNFDELN
Candida species are the most common cause of opportunistic fungal infection worldwide. Here we report the genome sequences of six Candida species and compare these and related pathogens and non-pathogens. There are significant expansions of cell wall, secreted and transporter gene families in pathogenic species, suggesting adaptations associated with virulence. Large genomic tracts are homozygous in three diploid species, possibly resulting from recent recombination events. Surprisingly, key components of the mating and meiosis pathways are missing from several species. These include major differences at the mating-type loci (MTL); Lodderomyces elongisporus lacks MTL, and components of the a1/2 cell identity determinant were lost in other species, raising questions about how mating and cell types are controlled. Analysis of the CUG leucine-to-serine genetic-code change reveals that 99% of ancestral CUG codons were erased and new ones arose elsewhere. Lastly, we revise the Candida albicans gene catalogue, identifying many new genes.
Candida dubliniensis is the closest known relative of Candida albicans, the most pathogenic yeast species in humans. However, despite both species sharing many phenotypic characteristics, including the ability to form true hyphae, C. dubliniensis is a significantly less virulent and less versatile pathogen. Therefore, to identify C. albicans-specific genes that may be responsible for an increased capacity to cause disease, we have sequenced the C. dubliniensis genome and compared it with the known C. albicans genome sequence. Although the two genome sequences are highly similar and synteny is conserved throughout, 168 species-specific genes are identified, including some encoding known hyphal-specific virulence factors, such as the aspartyl proteinases Sap4 and Sap5 and the proposed invasin Als3. Among the 115 pseudogenes confirmed in C. dubliniensis are orthologs of several filamentous growth regulator (FGR) genes that also have suspected roles in pathogenesis. However, the principal differences in genomic repertoire concern expansion of the TLO gene family of putative transcription factors and the IFA family of putative transmembrane proteins in C. albicans, which represent novel candidate virulence-associated factors. The results suggest that the recent evolutionary histories of C. albicans and C. dubliniensis are quite different. While gene families instrumental in pathogenesis have been elaborated in C. albicans, C. dubliniensis has lost genomic capacity and key pathogenic functions. This could explain why C. albicans is a more potent pathogen in humans than C. dubliniensis.
We present the diploid genome sequence of the fungal pathogen Candida albicans. Because C. albicans has no known haploid or homozygous form, sequencing was performed as a whole-genome shotgun of the heterozygous diploid genome in strain SC5314, a clinical isolate that is the parent of strains widely used for molecular analysis. We developed computational methods to assemble a diploid genome sequence in good agreement with available physical mapping data. We provide a whole-genome description of heterozygosity in the organism. Comparative genomic analyses provide important clues about the evolution of the species and its mechanisms of pathogenesis.
