Sommer Schneider, “MYH Genes and Development”
Mentor: Jennifer Gutzman, Biological Sciences
Poster #155

The MYH genes encode non-muscle myosin II proteins (NMIIs), which play important roles in cell migration, cell shape, and morphogenesis. There are three MYH genes in humans; MYH9, MYH10, and MYH14 and mutations in these genes cause a variety of disorders including thrombocytopenia, nephritis, visual defects, hearing loss, and cardiac abnormalities. However, the role of these genes in development and disease is not known. Therefore, we hypothesized that we could use zebrafish as a model system to elucidate their role in development and disease. We chose to study genes with high sequence homology to human, including zebrafish myh9a, myh9b, and myh10. We first examined the expression of myh9a, myh9b, and myh10 in the developing embryo up to 96 hours post fertilization (hpf). We found that both myh9b and myh10 are widely expressed during this time but myh9a had lower levels of expression and distribution. Next, are characterizing myh9a, myh9b and myh10 homozygous mutant embryos. myh9a and myh10 homozygous mutants appear normal through 6 days post fertilization (dpf) and have a similar probability of survival as wild-type animals up to 40 days, with no visible phenotypes. In contrast we found that myh9b homozygous mutants are semi-lethal and develop pericardial edema between 48- and 96-hours post fertilization. From this, we further hypothesize that myh genes may compensate for one another when one is mutated. To test this, we are generating and examining double mutant phenotypes. Our current results indicate that myh9a/myh9b double mutants exhibit more severe phenotypes that occur earlier in development, suggesting potential gene compensation within single mutants. We will continue to study double and triple mutants of the three genes to further explore the possibility of compensation and to further understand the role of these genes in development and disease.