(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
Warning: This entry is a compilation of different species or line or strain with more than 90% amino acide identity. You can retrieve all strain data
(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) Candida albicans SC5314: N, E.
Candida albicans WO-1: N, E.
Candida albicans P94015: N, E.
Candida albicans P37005: N, E.
Candida albicans GC75: N, E.
Candida albicans P57072: N, E.
Candida albicans P78048: N, E.
Candida albicans P37037: N, E.
Candida albicans 12C: N, E.
Candida albicans P87: N, E.
Candida albicans 19F: N, E.
Candida albicans L26: N, E.
Candida albicans P34048: N, E.
Candida albicans P57055: N, E.
Candida albicans P75063: N, E.
Candida albicans P76055: N, E.
Candida albicans P37039: N, E.
Candida albicans P75010: N, E.
Candida albicans P76067: N, E.
Candida albicans P75016: N, E.
Candida albicans Ca6: N, E.
Candida albicans P78042: N, E.
Candida albicans P60002: N, E.
Candida albicans Ca529L: N, E.
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 MHGTMITIDFFLKLVTLPYTVTKTVLQYYTVGTPYSRTNQEFRNSLWKNV LLSVQYHVSGNYKKENIKAVIYQPIDKVIAKFKTHPLASGLAHFGEKFDE YSYWIHKADTQGKVLIYIHGGGYLLNMFESQFVFVSALHYALDDHAAENT SILVVDYSLTMFDNVYPTQLYEHLVTYNNLVAQGYKDILLLGDSAGAHMS LSLARAIAYPEEAKQQLQQYNVSLDLPQPQALILVSPWVQPCTTPKLPPR HGCDVWGDLGAQDTSMGELYAGDNDKSFINNFLTFTNTNWDEHWKEVEAL NGNTLMIVGEREVLRDGVDDFYNIIKGGVEYYTEPGGIHAGLVYVECLDY ISKQGAERAIKGDFKDKFAYNLVAKFINERV
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.
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.
