Prenatal or childhood exposures to chronic stress can have lasting developmental effects that predispose the exposed individual to various diseases and more rapid aging during adulthood. Our current research seeks to understand the mechanisms mediating those effects. The overarching hypothesis being tested is that chronic induction of genetic and physiological stress responses during early development destabilizes the somatic genome, reducing the body's capacity for tissue homeostasis, repair, and regeneration.
One way that this is thought to occur is via stress-induced shortening of telomeres, the structures that maintain and protect the ends of chromosomes. Telomere shortening eventually leads to loss of genomic stability, which in turn induces cell senescence and/or death, resulting in loss of tissue homeostasis. We are using zebrafish as an experimental model to investigate these issues, as zebrafish are extraordinarily amenable to studies of early development, and the mechanisms through which chronic stress during early development affects telomere length and genomic stability are most likely conserved between zebrafish and humans.
Shusen Zhu, M.S., Research Assistant
Ellen Hartig, B.S., B.A., Research Assistant