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Mentor(s): Jennifer Schumacher and Griffin Chadwick 

Congenital heart defects (CHD) are developmental and functional abnormalities of an infant's heart at birth. CHD are the most common type of birth defect affecting approximately 1 in every 115 babies. Of all CHD, only about 13% have known causes. Zebrafish are used as a model organism to study congenital heart defects. Zebrafish serve as an excellent model to study CHD as they have the ability to survive without a functioning cardiovascular system for up to 4 days due to their thin skin which allows for oxygen diffusion. Zerbrafish have high conservation of signaling pathways and mechanisms allowing for translation into other models. Interaction between mesodermal precursors and their extracellular environment is critical to proper development. The mesoderm is a germ layer in the embryo where many organs derive from. Integrins are transmembrane receptor proteins that bind extracellular matrix proteins which leads to signal transduction of migration and proliferation. Integrins are made up of a combination of non-covalently bound alpha and beta subunits. Integrin ɑ4 and ɑ5 knockout has previously shown to lead to mesodermal derived tissue malformation. Presented here is a further understanding of how ɑ4 and ɑ5 knockout affect characterization of mesodermal percursor populations. Comparison of siblings and mutants was used to determine that there was no statistically significant differences in any precorusor populations other than the “left area” population. This work will bring a understanding of the cellular mechanisms that lead to heart defects during development.