A
Anja Forche
Researcher at Bowdoin College
Publications - 35
Citations - 4885
Anja Forche is an academic researcher from Bowdoin College. The author has contributed to research in topics: Candida albicans & Ploidy. The author has an hindex of 25, co-authored 35 publications receiving 4373 citations. Previous affiliations of Anja Forche include Duke University & University of Minnesota.
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Journal ArticleDOI
Evolution of pathogenicity and sexual reproduction in eight Candida genomes.
Geraldine Butler,Matthew D. Rasmussen,Michael F. Lin,Michael F. Lin,Manuel A. S. Santos,Sharadha Sakthikumar,Carol A. Munro,Esther Rheinbay,Esther Rheinbay,Manfred Grabherr,Anja Forche,Jennifer L. Reedy,Ino Agrafioti,Martha B. Arnaud,Steven Bates,Alistair J. P. Brown,Sascha Brunke,Maria C. Costanzo,David A. Fitzpatrick,Piet W. J. de Groot,David Harris,Lois L. Hoyer,Bernhard Hube,Frans M. Klis,Chinnappa D. Kodira,Nicola Lennard,Mary E. Logue,Ronny Martin,Aaron M. Neiman,Elissavet Nikolaou,Michael A. Quail,Janet Quinn,Maria C. Santos,Florian F. Schmitzberger,Gavin Sherlock,Prachi Shah,Kevin A. T. Silverstein,Marek S. Skrzypek,David R. Soll,Rodney Staggs,Ian Stansfield,Michael P. H. Stumpf,Peter E. Sudbery,Thyagarajan Srikantha,Qiandong Zeng,Judith Berman,Matthew Berriman,Joseph Heitman,Neil A. R. Gow,Michael C. Lorenz,Bruce W. Birren,Manolis Kellis,Manolis Kellis,Christina A. Cuomo +53 more
TL;DR: There are significant expansions of cell wall, secreted and transporter gene families in pathogenic species, suggesting adaptations associated with virulence in Candida albicans species.
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Aneuploidy and isochromosome formation in drug-resistant Candida albicans
TL;DR: Increase and decreases in drug resistance were strongly associated with gain and loss of this isochromosome, which bears genes expressing the enzyme in the ergosterol pathway targeted by azole drugs, efflux pumps, and a transcription factor that positively regulates a subset of efflux pump genes.
Journal ArticleDOI
A Mutation in Tac1p, a Transcription Factor Regulating CDR1 and CDR2, Is Coupled With Loss of Heterozygosity at Chromosome 5 to Mediate Antifungal Resistance in Candida albicans
Alix T. Coste,Vincent Turner,Françoise Ischer,Joachim Morschhäuser,Anja Forche,Anna Selmecki,Judith Berman,Jacques Bille,Dominique Sanglard +8 more
TL;DR: The mechanisms by which hyperactive alleles become homozygous was addressed by comparative genome hybridization and single nucleotide polymorphism arrays and indicated that loss of TAC1 heterozygosity can occur by recombination between portions of chromosome 5 or by chromosome 5 duplication.
Journal ArticleDOI
The Parasexual Cycle in Candida albicans Provides an Alternative Pathway to Meiosis for the Formation of Recombinant Strains
TL;DR: It is shown that deletion of SPO11 prevented genetic recombination between homologous chromosomes during the C. albicans parasexual cycle, suggesting that at least one meiosis-specific gene has been re-programmed to mediate genetic recombinations during the alternative paraseSexual life cycle of C.Albicans.
Journal ArticleDOI
An isochromosome confers drug resistance in vivo by amplification of two genes, ERG11 and TAC1.
TL;DR: The major mechanism by which i(5L) formation causes increased azole resistance is by amplifying two genes: ERG11 and TAC1.