Erika Shor, Ph.D.   

Shor Lab

Dr. Shor completed her Ph.D. under the mentorship of Dr. Rodney Rothstein at Columbia University and trained as a postdoctoral fellow in the labs of Dr. Catherine Fox at the University of Wisconsin-Madison and Dr. James Broach at Princeton University. As a graduate student, she received the National Science Foundation Graduate Student Fellowship, and as a postdoc, she was funded by fellowships from the Leukemia and Lymphoma Society and the American Cancer Society.

Dr. Shor’s graduate and postdoctoral research focused on understanding the mechanisms maintaining genome stability in the model eukaryote, baker’s yeast Saccharomyces cerevisiae. Driven by a strong interest in translating the insights obtained in a non-pathogenic model yeast to understanding the mechanisms operating in fungal pathogens that are relevant to human infections, she joined the laboratory of Dr. David Perlin, then at the Public Health Research Institute, New Jersey Medical School, as a research associate. In Dr. Perlin’s lab she began working on the opportunistic fungal pathogen Candida glabrata, which is a leading cause of invasive candidemia and candidiasis worldwide and which causes infections associated with high mortality.

Dr. Shor eventually joined the Center for Discovery and Innovation as a Research Assistant Member and was then promoted to Assistant Member leading the C. glabrata research program. In addition to the research, Dr. Shor runs the CDI Grant and Manuscript Editing Core.


Dr. Shor’s research program focuses predominantly on the mechanisms driving the emergence of drug resistance in C. glabrata, ranging from the mechanisms underpinning drug tolerance to those regulating genome instability and formation of genetic mutations conferring stable drug resistance. Some past and ongoing projects include:

  1. Developing a fluorescence-based mutation rate reporter assay in C. glabrata, which can be used in both drug-sensitive and drug-resistant clinical strains.

  2. Showing that the DNA damage checkpoint of C. glabrata is strongly attenuated relative to that of its close relative S. cerevisiae, which has implications for how this organism responds to DNA damage in vivo (e.g., in macrophages) and the development of genetic instability, including drug-resistant mutations.

  3. Identifying the host niches where genotypically sensitive but phenotypically resistant (a.k.a., drug-tolerant) C. glabrata cells survive despite treatment with cidal antifungal agents (such as echinocandins), thus forming a reservoir in which drug-resistant mutants can form. We are also focusing on elucidating the characteristics of such surviving persister cells, defining their evolutionary/mutational routes to resistance, and understanding the processes regulating genome stability and mutagenesis in these cells. 

Contact the Lab

For research or collaboration opportunities, contact

Mailing Address:
Center for Discovery and Innovation
111 Ideation Way
Nutley, NJ 07110

Google Scholar 
We use cookies to improve your site experience. By using this site,
you agree to our Terms & Conditions. Also, please read our Privacy Policy. Accept All CookiesLearn More