Past Research
Research conducted during my Ph.D. and postdoctoral work along with other published literature would suggest that the stress response which is activated during environmental perturbations is highly plastic which means it can be upregulated or downregulated based on a host of environmental inputs. Most vertebrates have elevated levels of corticosterone during the breeding season compared to other times of year (Fig. 1). The mechanism that control these seasonal changes remain poorly understood in free-living organism and is the future of research in our field. Our current research project aims to understand the mechanisms that control negative feedback that allow for this plasticity at the tissue level through changes in gene expression. Employment of molecular techniques will allow us to understand the regulatory mechanism that control hormone production, transport in the blood and signaling at the target tissue.
We collected two subspecies of white-crowned sparrow that are exposed to vastly different environmental condition across the annual cycle during breeding, postnuptial molt and wintering life history stages. The first is the long-distance migrant (Z.l. gambelii) that that we study in winter in Davis, California and in spring and summer on the North Slope of Alaska. The other is the non-migratory resident subspecies (Z.l. nuttalli) that breeds along the coast of California. Our data show that the migrant has much higher circulating levels of corticosterone during the breeding season compared to the resident for both males and females while no other differences have been detected during molt or wintering stages. Also note that these two subspecies will also allow us to investigate difference in gene expression associated with migration using the residents as a control group. We have also collected Lapland longspurs on the North Slope of Alaska during benign conditions in 2016, during the extreme year in 2013 (more details below in previous work) and during a snowstorm in 2016 that caused 90% reproductive failure in the region. During snowstorms and extreme weather events, we have shown that circulating corticosterone concentrations are elevated above their normal levels. Collection of tissues at each of these stages and under various conditions will all us to understand the mechanisms that allow for adaptive changes in stress physiology. We have collected brain, pituitary gland, adrenal glands, pectoralis muscle, gastrocnemius muscle, gonads, heart, fat, and liver to understand seasonal fluctuations in genes that are associated with stress. We intend to investigate other genes related to reproduction and regulators of metabolism but first we must meet the objectives for the grant.
Changes in gene expression of enzymes, transport proteins (CBG), receptors are important for stress signaling because they control steroid synthesis, transportation, modification by target tissues, receptor expression, and ultimately gene expression following receptor activation. Each of these points of regulation is likely to fluctuate across the breeding season to either sensitize or desensitize target tissues to circulating levels of corticosterone. We currently have done over 1400 RNA extractions and reverse transcriptions with another 400 remaining which is to be completed in October when I return to Scotland. The cDNA from the extracted samples are currently being analyzed using qPCR to quantify RNA expression in key tissues. My general future goals are to continue to unravel the mechanisms by which animals are adjusting to rapid climate change. It is my hope to expand this work using RNA-seq to understand how the transcriptome is changing in response to climate change and better understand the link between stress and other key physiological processes such as breeding and migration.
In addition, we conducted a series of laboratory and field based pharmacological experiments to further investigate how each receptor type and its expression in the various brain regions contribute to both basal and stress-induced levels of CORT. In addition, I am interested in how metabolic status has an influence on stress physiology. We have completed a series of food restriction experiments along with pharmacological manipulations to understand how stress is perceived during negative or positive energy balance and how stress hormone signaling aids in recovery post food restriction.
Changes in gene expression of enzymes, transport proteins (CBG), receptors are important for stress signaling because they control steroid synthesis, transportation, modification by target tissues, receptor expression, and ultimately gene expression following receptor activation. Each of these points of regulation is likely to fluctuate across the breeding season to either sensitize or desensitize target tissues to circulating levels of corticosterone. We currently have done over 1400 RNA extractions and reverse transcriptions with another 400 remaining which is to be completed in October when I return to Scotland. The cDNA from the extracted samples are currently being analyzed using qPCR to quantify RNA expression in key tissues. My general future goals are to continue to unravel the mechanisms by which animals are adjusting to rapid climate change. It is my hope to expand this work using RNA-seq to understand how the transcriptome is changing in response to climate change and better understand the link between stress and other key physiological processes such as breeding and migration.
In addition, we conducted a series of laboratory and field based pharmacological experiments to further investigate how each receptor type and its expression in the various brain regions contribute to both basal and stress-induced levels of CORT. In addition, I am interested in how metabolic status has an influence on stress physiology. We have completed a series of food restriction experiments along with pharmacological manipulations to understand how stress is perceived during negative or positive energy balance and how stress hormone signaling aids in recovery post food restriction.