"Fungus Man"
"Fungus Man"
Which lab are you currently working in?
I am a Research Associate in the White lab.
What are you doing at Seattle Biomedical Research Institute?
I dump reagents down the sink. Kidding! I investigate the mechanisms by which several pathogenic fungi become resistant to antifungal drugs. My job allows me to perform a really diverse set of experiments, such as sequencing the genomes of the organisms that cause athelete’s foot disease to performing clinical drug susceptibility tests with novel, antifungal compounds. I knock-out genes that may play a role in drug resistance in my spare time.
Where did you grow up?
I grew up in South Dayton, OH.
Where did you go to college? What did you like about your school?
I went to the University of Cincinnati. I started out without a major. As I really enjoyed my Biology classes, I ended up majoring in Biology. I liked the University of Cincinnati mainly because it is an urban university. There were many opportunities outside campus and had access to art, music and all the things a city can bring. It was far enough away from home that my parents never dropped by and close enough that I could take my laundry home and raid the fridge. Pretty inexpensive, too. During my undergrad, I worked in a lab. I started out washing dishes and making solutions and eventually worked my way up to having my own research projects. I studied Pneumocystis carinii.
What did you do after you graduated?
After graduation, I took the DAT and applied to dental school. I also worked at a dental clinic during this time and realized that working in the lab was a lot more fun.
Why did you apply to grad school?
I applied to graduate school because I realized that I enjoyed research. I did my graduate studies in the College of Medicine at the University of Cincinnati in the Department of Pathobiology and Molecular Medicine. This is a very unique program as graduate students train the first two quarters in the graduate school program and the next 3 quarters in the medical school program. For my thesis work, I looked at the pathogenic mechanisms of Aspergillus fumigatus(1-6).
Why did you come to Seattle Biomedical Research Institute?
After graduate school I came to Seattle Biomedical Research Institute because I wanted to join Ted White’s lab. My focus in my postgraduate research has been in resistance mechanisms of Candida albicans(7-16).
What are your hobbies outside of the lab?
Biking, reading, snowboarding, running, climbing, soccer, playing video games, fantasy football, and watching the Daily Show and the Colbert Report
From where you are now, what advise would you give to incoming and graduate BioQuest students?
Be sure to find what it is that you are really passionate about. Do not be afraid to mess up. You always learn from every mistake. And always remember that every day is a school day!
Publications:
- Identification of genes of Aspergillus fumigatus up-regulated during growth on endothelial cells.
- Cloning and expression of pkaC and pkaR, the genes encoding the cAMP-dependent protein kinase of Aspergillus fumigatus.
- Expression of the Aspergillus fumigatus rheb homologue, rhbA, is induced by nitrogen starvation.
- cAMP alteration of growth rate of Aspergillus fumigatus and Aspergillus niger is carbon-source dependent.
- Deletion of the Aspergillus fumigatus gene encoding the Ras-related protein RhbA reduces virulence in a model of Invasive pulmonary aspergillosis.
- Deletion of the regulatory subunit of protein kinase A in Aspergillus fumigatus alters morphology, sensitivity to oxidative damage, and virulence.
- Candida albicans UPC2 is transcriptionally induced in response to antifungal drugs and anaerobicity through Upc2p-dependent and -independent mechanisms.
- Micafungin activity against Candida albicans with diverse azole resistance phenotypes.
- Characterization of caspofungin susceptibilities by broth and agar in Candida albicans clinical isolates with characterized mechanisms of azole resistance.
- Polyene susceptibility is dependent on nitrogen source in the opportunistic pathogen Candida albicans.
- Tetracycline alters drug susceptibility in Candida albicans and other pathogenic fungi.
- cis-Acting elements within the Candida albicans ERG11 promoter mediate the azole response through transcription factor Upc2p.
- Drug-induced regulation of the MDR1 promoter in Candida albicans.
- Role of Candida albicans transcription factor Upc2p in drug resistance and sterol metabolism.
- The Candida albicans lanosterol 14-alpha-demethylase (ERG11) gene promoter is maximally induced after prolonged growth with antifungal drugs.
- Antifungal activity of fluconazole in combination with lovastatin and their effects on gene expression in the ergosterol and prenylation pathways in Candida albicans.
