Meeting Abstract
Mechanisms underlying the developmental origins of chronic adult diseases have yet to be determined. An important finding is that stress experienced during early life causes higher basal stress hormone levels, leading to later life behavioral, neural, and metabolic changes. To elucidate how stress hormones impart the lasting effects of stress, we use frog metamorphosis as a model. Amphibian metamorphosis is mediated by thyroid hormone (TH), and stress hormone Corticosterone (CORT) synergizes with TH to accelerate metamorphosis. The effects of CORT on development and subsequent altered stress hormone levels are conserved in tadpoles and humans. Towards the overall goal of understanding the mechanisms of permanent effects of stress on development, I am characterizing Str. 34945, the only known CORT-response element not also regulated by TH. The Str. 34945 sequence maps onto the Xenopus tropicalis genome in between the genes ush1g (Usher syndrome 1G) and fads6 (fatty acid desaturase 6), but it is unclear if it is part of one of these genes or if it is a noncoding RNA sequence. Based on our data, this gene is ush1g. In an effort to determine how and where Str. 34945 is expressed in the tadpole, we treated the animals with CORT and measured Str. 34945 expression via qPCR. When tadpoles were treated with CORT for 24 hours we found Str. 34945 is upregulated in the whole tail, tail muscle, lungs, liver, and heart; it is not expressed in the brain or kidney. Furthermore, we show Str. 34945 is consistent with the only other known CORT response gene and shows the expected expression profile based on normal CORT changes through metamorphosis. Our results demonstrate that Str. 34945 can be a unique tool to specifically detect the presence of CORT.
