Evolution of pathogenicity and sexual reproduction in eight Candida genomes

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.publishe

Mapping quantitative trait loci responsible for resistance to sheath blight in rice

Rice sheath blight (ShB), caused by the soilborne pathogen Rhizoctonia solani, annually causes severe losses in yield and quality in many rice production areas worldwide. Jasmine 85 is an indica cultivar that has proven to have a high level of resistance to this pathogen. The objective of this study was to determine the ability of controlled environment inoculation assays to detect ShB resistance quantitative trait loci (QTLs) in a cross derived from the susceptible cv. Lemont and the resistant cv. Jasmine 85. The disease reactions of 250 F5 recombinant inbred lines (RILs) were measured on the seedlings inoculated using microchamber and mist-chamber assays under greenhouse conditions. In total, 10 ShBQTLs were identified on chromosomes 1, 2, 3, 5, 6, and 9 using these two methods. The microchamber method identified four of five new ShBQTLs, one on each of chromosomes 1, 3, 5, and 6. Both microchamber and mist-chamber methods identified two ShB-QTLs, qShB1 and qShB9- 2. Four of the ShB-QTLs or ShB-QTL regions identified on chromosomes 2, 3, and 9 were previously reported in the literature. The major ShB-QTL qShB9-2, which cosegregated with simple sequence repeat (SSR) marker RM245 on chromosome 9, contributed to 24.3 and 27.2% of total phenotypic variation in ShB using microchamber and mistchamber assays, respectively. qShB9-2, a plant-stage-independent QTL, was also verified in nine haplotypes of 10 resistant Lemont/Jasmine 85 RILs using haplotype analysis. These results suggest that multiple ShBQTLs are involved in ShB resistance and that microchamber and mistchamber methods are effective for detecting plant-stage-independent QTLs. Furthermore, two SSR markers, RM215 and RM245, are robust markers and can be used in marker-assisted breeding programs to improve ShB resistance

Targeted changes of the cell wall proteome influence [i]Candida albican[/i]s ability to form single- and multi-strain biofilms

International audienceBiofilm formation is an important virulence trait of the pathogenic yeast Candida albicans. We have combined gene overexpression, strain barcoding and microarray profiling to screen a library of 531 C. albicans conditional overexpression strains (similar to 10% of the genome) for genes affecting biofilm development in mixed-population experiments. The overexpression of 16 genes increased strain occupancy within a multi-strain biofilm, whereas overexpression of 4 genes decreased it. The set of 16 genes was significantly enriched for those encoding predicted glycosylphosphatidylinositol (GPI)modified proteins, namely Ihd1/Pga36, Phr2, Pga15, Pga19, Pga22, Pga32, Pga37, Pga42 and Pga59; eight of which have been classified as pathogen-specific. Validation experiments using either individually- or competitively-grown overexpression strains revealed that the contribution of these genes to biofilm formation was variable and stage-specific. Deeper functional analysis of PGA59 and PGA22 at a single-cell resolution using atomic force microscopy showed that overexpression of either gene increased C. albicans ability to adhere to an abiotic substrate. However, unlike PGA59, PGA22 overexpression led to cell cluster formation that resulted in increased sensitivity to shear forces and decreased ability to form a single-strain biofilm. Within the multi-strain environment provided by the PGA22-non overexpressing cells, PGA22-overexpressing cells were protected from shear forces and fitter for biofilm development. Ultrastructural analysis, genome-wide transcript profiling and phenotypic analyses in a heterologous context suggested that PGA22 affects cell adherence through alteration of cell wall structure and/or function. Taken together, our findings reveal that several novel predicted GPI-modified proteins contribute to the cooperative behaviour between biofilm cells and are important participants during C. albicans biofilm formation. Moreover, they illustrate the power of using signature tagging in conjunction with gene overexpression for the identification of novel genes involved in processes pertaining to C. albicans virulence