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The human pathogenic yeast Candida parapsilosis has gained significant importance over the past decades as one of the principal causes of fungal bloodstream infections. Isolates of C. parapsilosis are known to be able to switch between several different colony morphologies in vitro, which are correlated with different cell shapes, altered cell surface properties, and thus different capacities to form biofilms on indwelling medical devices. In a set of six clinical specimens from a single surgery patient yielding stable smooth- as well as crepe-morphology isolates, we investigated the differences between five of them on a phenotypic and genomic level. In contrast to the initial assumption that they were switched forms of a clonal strain, karyotyping and genome sequencing showed that the patient was colonized by at least three distinct linages. Statistical analysis placed these groups distantly across the population of C. parapsilosis. Interestingly the single blood culture isolate was of smooth morphology and matched with an isolate from the patient’s nose of similar morphology. Strong variation between the isolates was seen in adhesin-encoding genes, where repeat regions showed significant variation in length and repeat-numbers, most strikingly in HWP1 of the smooth isolates. Although no differences in drug susceptibility were evident, the high phylogenetic distance separating the individual strains highlights the need for testing of multiple colonies in routine practice. The absence of biofilm formation in the blood stream isolate indicates a lack of respective adhesins in the cell wall, in turn pointing toward lack of adhesion as a positively contributing factor for dissemination., This study was funded through the FP7-PEOPLE-2013-ITN—Marie-Curie Action: “Initial Training Networks”: Molecular Mechanisms of Human Fungal Pathogen Host Interaction, ImResFun, Project ID: 606786, to AG, TG, OB, and UG., Peer Reviewed, Postprint (published version)

Theglobalepidemiologyoffungalinfectionsischanging.Whileoverall,Candidaalbicans remainsthemost commonpathogen; severalinstitutions inEurope,AsiaandSouthAmericahavereportedtherapidemergence to predominance of Candida parapsilosis. This mini-review examines the impact of gene deletions achievedinC.parapsilosis thathavebeenpublishedtodate.Themolecular approaches togenedisruption in C. parapsilosis and the molecularly characterized genes to date are reviewed. Similar to C. albicans, factors in?uencing virulence in C. parapsilosis include adherence, bio?lm formation, lipid metabolism, and secretion of hydrolytic enzymes such as lipases, phospholipases and secreted aspartyl proteinases. Developmentof a targetedgenedeletionmethodhasenabledtheidenti?cationof severaluniqueaspects of C. parapsilosis genes that play a role in host�pathogen interactions � CpLIP1, CpLIP2, SAPP1a, SAPP1b, BCR1, RBT1, CpFAS2, OLE1, FIT-2., La epidemiología mundial de las infecciones fúngicas está cambiando. Aunque Candida albicans sigue siendo el patógeno más común, varios centros en Europa, Asia y Sudamérica han descrito la rápida emergencia de Candida parapsilosis, que ha terminado por predominar. La presente revisión examina la in?uenciade lasdeleciones genéticasproducidas enC. parapsilosisque sehanpublicadohasta la fecha. Se revisan las estrategias moleculares de la alteración de genes de C. parapsilosis y los genes caracterizados molecularmente hasta la fecha. Al igual que en C. albicans, los factores que in?uyen en la virulencia de C. parapsilosis incluyen la adherencia,formación de biopelículas, el metabolismo de lípidos y la secreción de enzimas hidrolíticas, como lipasas,fosfolipasas y aspartilproteinasas. El desarrollo de unmétodo de deleción génica dirigido ha permitido la identi?cación de varios aspectos exclusivos de los genes de C. parapsilosis que participan en las interacciones huésped-patógeno-CpLIP1, CpLIP2, SAPP1a, SAPP1b, BCR1, RBT1, CpFAS2, OLE1, FIT-2

Convergent evolution is common throughout the tree of life, but the molecular mechanisms causing similar phenotypes to appear repeatedly are obscure. Yeasts have arisen in multiple fungal clades, but the genetic causes and consequences of their evolutionary origins are unknown. Here we show that the potential to develop yeast forms arose early in fungal evolution and became dominant independently in multiple clades, most likely via parallel diversification of Zn-cluster transcription factors, a fungal-specific family involved in regulating yeast-filamentous switches. Our results imply that convergent evolution can happen by the repeated deployment of a conserved genetic toolkit for the same function in distinct clades via regulatory evolution. We suggest that this mechanism might be a common source of evolutionary convergence even at large time scales.

Convergent evolution is common throughout the tree of life, but the molecular mechanisms causing similar phenotypes to appear repeatedly are obscure. Yeasts have arisen in multiple fungal clades, but the genetic causes and consequences of their evolutionary origins are unknown. Here we show that the potential to develop yeast forms arose early in fungal evolution and became dominant independently in multiple clades, most likely via parallel diversification of Zn-cluster transcription factors, a fungal-specific family involved in regulating yeast-filamentous switches. Our results imply that convergent evolution can happen by the repeated deployment of a conserved genetic toolkit for the same function in distinct clades via regulatory evolution. We suggest that this mechanism might be a common source of evolutionary convergence even at large time scales.