Several areas of the vertebrate brain are involved in facilitating and inhibiting the production of sexual behaviors and displays. In the laboratory, a higher rate of sexual displays is correlated with a larger ventral posterior amygdala (VPA), an area of the brain involved in the expression of sexual display behaviors, as well as larger VPA neuronal somas. However, it remains unclear if individuals in the field reflect similar patterns, as there are likely many more selective pressures in the field that may also modulate the VPA architecture. In this study, we examined variation in VPA volume and neuron soma volume in wild-caught common side-blotched lizards (Uta stansburiana) from two different populations. In a population from Nevada, males experience high predation pressure and have decreased sexual display rates during the breeding season, whereas a population in Oregon has lower levels of predation and higher rates of male sexual displays. We found that wild-caught males from the population with lower display rates also exhibited decreased VPA volume and VPA neuron cell soma volume, which may suggest that decreased display rate, possibly due to increased predation rate, covaries with VPA attributes.

The farnesoid X‐receptor (FXR), a nuclear receptor, is a ligand‐regulated transcription factor that regulates bile acid, lipid, and glucose metabolism. FXR consists of a ligand‐binding domain (LBD), that bind small lipophilic ligands, and a DNA binding domain (DBD) that targets specific areas of DNA called FXR response elements (FXRE). When ligands bind to the LBD, allosteric structural changes occur in the DBD and affect the DNA binding preferences. Once bound to FXREs, ligand‐bound FXR regulates the transcription of specific genes. While the natural ligands of FXR are bile acids, many synthetic ligands have also been developed to regulate FXR. Previous studies have shown that structurally similar FXR ligands activate FXR in a gene‐specific fashion. However, it is not clear how these similar FXR ligands achieve such varying effects on DNA binding preferences. My project focuses on a structurally related group of synthetic FXR ligands (fexaramine, fexarine and fexarene) to understand how ligand structure impacts FXR‐DNA binding. To investigate how modifications in the ligand scaffold regulate FXR transcriptional activity, I am performing dual‐luciferase assays to measure the transcription in a large set of FXRE‐driven promoters.