title: Increased virulence and competitive advantage of a/alpha over a/a or alpha/alpha offspring conserves the mating system of Candida albicans.
abstract: The majority of Candida albicans strains in nature are a/alpha and must undergo homozygosis to a/a or alpha/alpha to mate. Here we have used a mouse model for systemic infection to test the hypothesis that a/alpha strains predominate in nature because they have a competitive advantage over a/a and alpha/alpha offspring in colonizing hosts. Single-strain injection experiments revealed that a/alpha strains were far more virulent than either their a/a or alpha/alpha offspring. When equal numbers of parent a/alpha and offspring a/a or alpha/alpha cells were co-injected, a/alpha always exhibited a competitive advantage at the time of extreme host morbidity or death. When equal numbers of an engineered a/a/alpha2 strain and its isogenic a/a parent strain were co-injected, the a/a/alpha2 strain exhibited a competitive advantage at the time of host morbidity or death, suggesting that the genotype of the mating-type (MTL) locus, not associated genes on chromosome 5, provides a competitive advantage. We therefore propose that heterozygosity at the MTL locus not only represses white-opaque switching and genes involved in the mating process, but also affects virulence, providing a competitive advantage to the a/alpha genotype that conserves the mating system of C. albicans in nature.
authors.affiliation: Department of Biological Sciences, The University of Iowa, Iowa City, 52242-1324, USA.
authors.forename: Shawn R
authors.initials: SR
authors.lastname: Lockhart
authors.forename: Wei
authors.initials: W
authors.lastname: Wu
authors.forename: Joshua B
authors.initials: JB
authors.lastname: Radke
authors.forename: Rui
authors.initials: R
authors.lastname: Zhao
authors.forename: David R
authors.initials: DR
authors.lastname: Soll
mesh_terms: D000818:Animals; D000946:Antigens, Fungal; D001667:Binding, Competitive; D002176:Candida albicans / Q000235:genetics* / Q000472:pathogenicity*; D004195:Disease Models, Animal; D005656:Fungal Proteins / Q000502:physiology; D015966:Gene Expression Regulation, Fungal; D005800:Genes, Fungal; D049770:Genes, Mating Type, Fungal; D005818:Genetic Engineering; D005838:Genotype; D006579:Heterozygote; D051379:Mice; D008957:Models, Genetic; D010641:Phenotype; D016133:Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014774:Virulence
chemical_list: D000946:Antigens, Fungal; D005656:Fungal Proteins