This summer has been an eventful and productive one for the Anderson Lab! Here is a brief overview of what we were up to:
Joshua Wang – Joshua Wang joined us from Brown University where he worked with Dr. Anderson on a variety of bioinformatics projects.
Delanie Baker – Delanie Baker was with us for a few months through the NSF REU in the Department of Molecular Biology at The Ohio State University.
Midwest Neglected Infectious Disease 2017 – The MNID meeting is the only regional meeting in the Midwest that features forefront research focused on the pathogenesis of fungal and parasitic diseases. This meeting fills an important void, as the parasitic and fungal diseases, while crucially important; do not receive sufficient “press” at many major biology meetings. Over the past years the meetings have included 100-130 scientists from seven states; Wisconsin, Illinois, Indiana, Michigan, Ohio, Iowa, and Missouri.
Robert Fillinger – Development of quantitative trait loci (QTL) mapping in Candida albicans
Matthew Dunn – Functional diversification accompanies telomere-associated (TLO) gene family expansion in Candida albicans
We would like to welcome Joshua Wang to the lab! Joshua comes to us from Brown University where he worked with Dr. Anderson on a variety of bioinformatics projects. He is currently in the process of preparing applications for medical school this upcoming year. We look forward to the enhanced skill set he brings the Anderson Lab and Ohio State as a whole!
Exploration of genomic sequences of C. albicans to pinpoint biomarkers correlated with specific phenotypes and identity expression profiles for previously undescribed gene networks.
Brown University – B.S. in Biology
(Computer Sciences track)
A special welcome to Delanie Baker who has been with us for a few months this summer through the NSF REU in the Department of Molecular Biology at The Ohio State University. Delanie has been working alongside Robert Fillinger on target loci for fluconazole resistance and the filamentation phenotype in C. albicans.
Phenotyping Candida albicans strains for the identification of quantitative trait loci involved in filamentation and fluconazole resistance.
Bachelors of Science in Microbiology at Ohio Wesleyan University
A chromosome 4 trisomy contributes to increased fluconazole resistance in a clinical isolate of Candida albicans. – PubMed – NCBI
Candida albicans is an important opportunistic fungal pathogen capable of causing both mucosal and disseminated disease. Infections are often treated with fluconazole, a front-line antifungal drug that targets the biosynthesis of ergosterol, a major component of the fungal cell membrane. Resistance to fluconazole can arise through a variety of mechanisms, including gain-of-function mutations, loss of heterozygosity events and aneuploidy. The clinical isolate P60002 was found to be highly resistant to azole-class drugs, yet lacked mutations or chromosomal rearrangements known to be associated with azole resistance. Transcription profiling suggested that increased expression of two putative drug efflux pumps, CDR11 and QDR1, might confer azole resistance. However, ectopic expression of the P60002 alleles of these genes in a drug-susceptible strain did not increase fluconazole resistance. We next examined whether the presence of three copies of chromosome 4 (Chr4) or chromosome 6 (Chr6) contributed to azole resistance in P60002. We established that Chr4 trisomy contributes significantly to fluconazole resistance, whereas Chr6 trisomy has no discernible effect on resistance. In contrast, a Chr4 trisomy did not increase fluconazole resistance when present in the standard SC5314 strain background. These results establish a link between Chr4 trisomy and elevated fluconazole resistance, and demonstrate the impact of genetic background on drug resistance phenotypes in C. albicans.
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