Shannon Mcconahy, “Investigating the Role of MYH9 Mutations in Ciliary Function and Development Using Zebrafish Models”
Mentor: Jennifer Gutzman, Biological Sciences, Letters & Science (College of)
Poster #170
Proper function of sensory cilia is essential for various physiological processes, including sensory perception and movement. Disruption of cilia structure or function can lead to significant developmental or behavioral abnormalities, impacting survival and health. This research project explores the role of the myh9b gene in zebrafish sensory systems, focusing on its implications in the development of MYH9-Related Diseases, which are associated with defects in ciliated organs in humans. Although MYH9 mutations in humans are known to cause diseases, its specific role in early vertebrate development remains poorly understood. The MYH9 gene encodes for a non-muscle myosin heavy chain protein (NMIIA) that is vital for cell movement, cell division, and cellular structure. Similarly, its counterpart in zebrafish, myh9b, has an essential role in embryonic development and tissue morphogenesis. We hypothesize that myh9b is required for development of sensory cilia and that mutations in myh9b may lead to impaired escape behaviors critical for survival. To test this, we are using behavioral assays in wild-type and mutant zebrafish larvae at 72 hours post fertilization. We examine the touch response of zebrafish embryos by gently poking their tails and ears to observe their escape behaviors. According to our preliminary research, mutations in myh9b affect the zebrafish embryos’ ability to escape. We further hypothesize that this may be caused by abnormal sensory cilia development in these mutants. This highlights a novel and critical role of myh9b in vertebrate sensory development and suggests potential parallels with ciliary dysfunction in human MYH9-Related Diseases.