Developmental birth defects emerge due to abnormalities in the formation and growth of embryonic tissues. Congenital heart defects are the most common developmental defect in humans. This condition can affect the tissue within the heart and the surrounding greater vessels. Zebrafish are used to study these defects because their anatomy provides a similar and simpler version of the mammalian heart and great vessels. Retinoic acid is a known developmental coordinator of heart and great vessel patterning in humans, mice, and zebrafish. However, the role of endogenous retinoic acid in formation of the zebrafish ventral aorta, which carries blood away from the heart, has not been investigated. To test the role of endogenous retinoic acid in ventral aorta development, we used the retinoic acid inhibitor 4-(Diethylamino)benzaldehyde (DEAB). Zebrafish embryos carrying the kdrl:GFP transgene to mark blood vessels were treated with DEAB starting at 26 hpf. The effects of the treatment were analyzed in 50 hpf and 72 hpf embryos that were fixed and processed for immunostaining to visualize GFP. Dimethyl sulfoxide (DMSO) was used as a control treatment. When compared to the control, embryos treated with DEAB displayed a lengthened posterior branch of the ventral aorta and abnormal fusion of the anterior branch of the ventral aorta. This abnormal fusion can result in a significantly shorter anterior branch of the ventral aorta compared to the control. Our findings suggest that endogenous retinoic acid regulates the fusion of the anterior branch and restricts the lengthening of the posterior branch of the ventral aorta. Overall, the irregular development of the ventral aorta due to DEAB treatment reveals for the first time the importance of endogenous retinoic acid signaling in the development of the ventral aorta in zebrafish.
Author(s): Allison Small, Biology Major
Advisor(s): Jennifer Schumacher, Department of Biology
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