Presenter(s): Samuel Ahlquist – Human Physiology
Co presenter(s): Whitney Olivia
Faculty Mentor(s): Charles Kimmel
Poster 88
Research Area: Biology
This study assesses the interaction between two genes, fras1 and ezh2, in zebrafish craniofacial patterning. The Fras1 protein stabilizes facial development and is studied to understand Fraser syndrome in humans. Ezh2 is a protein subunit of a repressive complex that is important for early embryonic development and essential for tissue maintenance. Ezh2 is explored because of its role in controlling epigenetics, which is a background that can affect the expression of genes. Loss of function in these two genes individually results in mild reduction in the opercular bone (OP). We therefore hypothesized that the interaction between ezh2 and fras1 in double mutants will result in more severe reduction in OP bone size. Zebrafish embryos were stained to assess bone morphology and each set was phenotypically separated into WT, single, and double mutant groups using key phenotypes. The embryos will be genotypically verified through PCR in this ongoing study. As predicted, the double mutants displayed more severe reduction in the OP bone when compared to the single mutants. We concluded that the double mutants displayed a synergistic effect for the OP bone as the result appears more severe than both single mutants combined. This study suggests that changes in epigenetics, in this case loss of ezh2 function, influences the severity of the fras1 phenotype which could also influence the degree of severity of Fraser syndrome in humans.