Environmental interactions play a critical role in the quality-of-life of a living organism, but the molecular nature of how the environment influences alterations within an individual is largely unknown.
Evidence suggests that these interactions induce changes at molecular, cellular and system levels that can result in life-long or even multi-generational changes to physiology or behavior. The vertebrate stress response system (SRS) is a diverse suite of neuronal, endocrine, and autonomic response mechanisms that play key roles in environmental interactions.
The clinical significance of stress-aggravated disorders is extremely high. Stress-aggravation can occur when a stressor is too strong (acute), occurs too often (chronic), or alters long-term responses to future stressors through neural network or epigenetic transcriptome changes.
The gene and environment interactions of the SRS and its role in disease progression depend on heritable genetic factors, life priming events, and later life events that may trigger disease onset. Normal life-priming promotes adaptive resilience to stressors. However, both low and high exposures to stress can be maladaptive to the developing SRS.
Our research goals include deploying zebrafish, a vertebrate model organism with genetic tractability, to study the vertebrate stress response system and answer questions such as:
What genes play a role in modulating the stress response?
How are early environmental stimuli recorded to create long-lasting changes in the biology of animals?
How do stressors and the body's response to stressors contribute to the onset and severity of disease?