Characterization of Neural Crest Cell Migration in the Absence of Cabin1 in Developing Zebrafish
Mentor 1
Ava J. Udvadia
Location
Union Wisconsin Room
Start Date
27-4-2018 1:00 PM
Description
Craniofacial anomalies are a prominent issue in newborns. In order to study a possible cause for such events, we are looking further into the behavior of neural crest cells (NCCs). NCCs are progenitor cells found in early development, which eventually give rise to diverse populations of specialized cells including those that make up craniofacial cartilage. Their ultimate function is determined by their location after they migrate out from the developing nervous system, where they originate, into the rest of the body. The protein Cabin1 is a transcriptional repressor, and it has not been researched to a great extent in the context of craniofacial development. However, previous work from Dr. Udvadia’s lab showed that larval zebrafish with reduced expression of the Cabin1 protein developed craniofacial deformities. Therefore, we hypothesize that a loss of the protein Cabin1 affects the migration of neural crest cells. To test our hypothesis, we are working with zebrafish strains that contain deletions in the Cabin1 gene, which prevent synthesis of functional Cabin1 protein. The Cabin1 mutant strains have been outcrossed with transgenic reporter strains, which will allow us to follow the migration of NCCs and chondrocytes in live developing embryos. The transgenic reporter strains express green fluorescent protein (GFP) in the developing NCCs and chondrocytes. With the use of a fluorescent microscope we will be able to capture images of the NCCs and chondrocytes at the larval stage of fish during craniofacial cartilage development. The movement of the NCCs and the morphology of the cartilage will be analyzed using the ImageJ and MorphoJ computer programs. The analytical comparison of the images will elucidate the effect of the loss of Cabin1 in the movement of NCCs as they form chondrocytes. The findings from this study have the potential to explain new mechanisms underlying craniofacial birth defects in humans.
Characterization of Neural Crest Cell Migration in the Absence of Cabin1 in Developing Zebrafish
Union Wisconsin Room
Craniofacial anomalies are a prominent issue in newborns. In order to study a possible cause for such events, we are looking further into the behavior of neural crest cells (NCCs). NCCs are progenitor cells found in early development, which eventually give rise to diverse populations of specialized cells including those that make up craniofacial cartilage. Their ultimate function is determined by their location after they migrate out from the developing nervous system, where they originate, into the rest of the body. The protein Cabin1 is a transcriptional repressor, and it has not been researched to a great extent in the context of craniofacial development. However, previous work from Dr. Udvadia’s lab showed that larval zebrafish with reduced expression of the Cabin1 protein developed craniofacial deformities. Therefore, we hypothesize that a loss of the protein Cabin1 affects the migration of neural crest cells. To test our hypothesis, we are working with zebrafish strains that contain deletions in the Cabin1 gene, which prevent synthesis of functional Cabin1 protein. The Cabin1 mutant strains have been outcrossed with transgenic reporter strains, which will allow us to follow the migration of NCCs and chondrocytes in live developing embryos. The transgenic reporter strains express green fluorescent protein (GFP) in the developing NCCs and chondrocytes. With the use of a fluorescent microscope we will be able to capture images of the NCCs and chondrocytes at the larval stage of fish during craniofacial cartilage development. The movement of the NCCs and the morphology of the cartilage will be analyzed using the ImageJ and MorphoJ computer programs. The analytical comparison of the images will elucidate the effect of the loss of Cabin1 in the movement of NCCs as they form chondrocytes. The findings from this study have the potential to explain new mechanisms underlying craniofacial birth defects in humans.
