PhD Candidate – Started 2013
Hometown: Davis, CA
Advisor/Lab: Chris Bradfield
Research Interests: Physiological role of the aryl hydrocarbon receptor repressor.
University of California-Davis (2009-2013)
Bachelors of Environmental Toxicology (2013)
Watching sports, hiking, tennis, racquetball, sailing, basketball, frisbee related stuff, eating, and napping
Why I Joined METC
METC has a wide array of researchers in a multitude of fields that students are able to work with. As someone who wasn’t sure exactly what I wanted to work on, it was a good fit as it would expose me to the many different areas of toxicology.
The aryl hydrocarbon receptor (AHR) is a transcription factor activated by various compounds. Once activated by a ligand, AHR will translocate to the nucleus and bind to ARNT. This AHR-ARNT complex is then able to bind to DNA and cause the upregulation of certain genes. AHRR (aryl hydrocarbon receptor repressor) expression is upregulated by the AHR-ARNT heterodimer. AHRR will dimerize with ARNT and compete with the AHR-ARNT heterodimer to bind to dioxin response elements (DRE). In this way, AHRR forms a negative feedback loop by repressing AHR mediated gene activity. Because of this, AHRR is associated with AHR activity. We are currently examining AHRR expression in mouse embryos and new born pups using mice transfected with a Lac-Z reporter gene to determine where and at what time points AHRR is being transcribed. Using this method, we determined that AHRR was expressed in the kidney and testis. We also sought to determine which ligands of AHR would induce AHRR. We also have been testing different ligands to see if they elicit similar inductions of AHRR.
In addition to examining tissues for AHRR expression, a concurrent project is generating an AHRR -/- mouse. This mouse can be used to examine the long term effect of AHR activity and may possibly shed light on the reason for the differential effects of various ligands of AHR. The AHRR -/- mouse was crossed with a Cyp1a1, Cyp1a2, and Cyp1b1 triple knockout to further examine the multitude of responses of AHR. This model will also provide means to investigate possible endogenous ligands of AHR. In addition, this model will provide information on the mechanism of action of dioxin and other environmental toxins that act through AHR.