(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 acid 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.
Candida tropicalis MYA-3404: N, E.
Candida dubliniensis CD36: 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 MTLEKNRHANKGTSWTWMIYKFVVGVITVAILVLFITQKSVSQAQDKLRV EQQAIFSDQDTLQLKHIFHHGTGPKNYRLHRRLDITSEYLAKHQPYFTTL TQQLSKPVLEEHIASDNLDKIYQQSDWPEIHKGKNPFSIELPFKKADSEA TRLKERNTPNFIESYLNYARDIKGDAQILNRINLDWIHDEIKVPNVTDRD TVVTLATISSNAYVRYPKDDDEKRKSDWIDLGDWDPNREDDDVNFGWDDI GLRGHVFVSKDNKTVVIGIKGTSGAGLPGGGSDETGGNDKTNDNLLFSCC CARISYMWTTVCDCYEKTYTCNQDCLEKELRKEDKYYQAVLELYRNVTDI YPPESTDIWVTGHSLGGALASLLGRTFGLPAVAFEAPGEMLATRRLHLPS PPGLPQHMENIWHFGNTADPIYMGVCNGASSTCNLAGYAMETTCHTGLQC VYDVVTDKGWSVNLLNHRIHTVIDDIILTYNETAPCAPSPPCRDCFNWRF VAHDDNEKDEPKLPNPLRSSSKSTLSTKTTSLKSSSTYSGSTSSSTVTKT TQTSPISSASPTDQDPPKKCLKRTWYGWCTKWGYYDDDDDEDTFERK
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.
Title: A Candida albicans genome project: cosmid contigs, physical mapping, and gene isolation Tait E, Simon MC, King S, Brown AJ, Gow NA, Shaw DJ Ref: Fungal Genet Biol, 21:308, 1997 : PubMed
A new project to map the genome of the pathogenic fungus, Candida albicans, has been started. The entire genome was cloned as 5088 cosmids, stored in individual microtiter plate wells. DNA was prepared and fingerprinted using restriction digestion, fluorescent labeling, and analysis on an ABI sequencer. These data are being used to construct contigs of the genome. Simultaneously, a DNA pooling system has been set up, suitable for PCR-based isolation of cosmids containing any known gene. Ultimately, these approaches will lead to the creation of a physically based map of the C. albicans genome, providing the means to localize precisely all the genes, act as a substrate for genome sequencing projects, and provide probes for future studies of genome rearrangement and comparative genomics.
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.
Title: A Candida albicans genome project: cosmid contigs, physical mapping, and gene isolation Tait E, Simon MC, King S, Brown AJ, Gow NA, Shaw DJ Ref: Fungal Genet Biol, 21:308, 1997 : PubMed
A new project to map the genome of the pathogenic fungus, Candida albicans, has been started. The entire genome was cloned as 5088 cosmids, stored in individual microtiter plate wells. DNA was prepared and fingerprinted using restriction digestion, fluorescent labeling, and analysis on an ABI sequencer. These data are being used to construct contigs of the genome. Simultaneously, a DNA pooling system has been set up, suitable for PCR-based isolation of cosmids containing any known gene. Ultimately, these approaches will lead to the creation of a physically based map of the C. albicans genome, providing the means to localize precisely all the genes, act as a substrate for genome sequencing projects, and provide probes for future studies of genome rearrangement and comparative genomics.
