Examining genetic interactions between the akirin and MTA-Like loci for cardiac and skeletal muscle development
Disciplines
Developmental Biology
Abstract (300 words maximum)
Congenital heart disease is a cardiac abnormality that is caused due to improper development of the heart. The severity of heart defects this disease produces can range from minor to severe, with some of the most severe cases being deformed or missing heart valves. To better understand the genetic mechanism(s) behind cardiac and skeletal muscle development, the Nowak lab has identified several genetic loci that have an impactful role in embryonic heart development. In previous work, our data suggests that Akirin works with the Nucleosome Remodeling and Deacetylase complex for proper heart and skeletal muscle development.
For the purposes of this project one of the subunits of the NuRD complex, MTA-Like, will be examined and how it plays a critical role in cardiac development, cardiac function and skeletal muscle development. To achieve this goal, we recombined the toll-cGFP transgene onto an MTA-Like mutant and analyzed skeletal patterning and cardiac function in akirin, MTA-Like double heterozygous mutant embryos. To properly analyze these mutations, live confocal imaging was used to record and analyze heartbeats that are produced from the recombination of the MTA-Like and Akirin cross. Additionally, we quantified the number and type of skeletal muscle defects observed in the akirin,+/+,MTA-Like double heterozygous mutant embryos.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Scott Nowak
Examining genetic interactions between the akirin and MTA-Like loci for cardiac and skeletal muscle development
Congenital heart disease is a cardiac abnormality that is caused due to improper development of the heart. The severity of heart defects this disease produces can range from minor to severe, with some of the most severe cases being deformed or missing heart valves. To better understand the genetic mechanism(s) behind cardiac and skeletal muscle development, the Nowak lab has identified several genetic loci that have an impactful role in embryonic heart development. In previous work, our data suggests that Akirin works with the Nucleosome Remodeling and Deacetylase complex for proper heart and skeletal muscle development.
For the purposes of this project one of the subunits of the NuRD complex, MTA-Like, will be examined and how it plays a critical role in cardiac development, cardiac function and skeletal muscle development. To achieve this goal, we recombined the toll-cGFP transgene onto an MTA-Like mutant and analyzed skeletal patterning and cardiac function in akirin, MTA-Like double heterozygous mutant embryos. To properly analyze these mutations, live confocal imaging was used to record and analyze heartbeats that are produced from the recombination of the MTA-Like and Akirin cross. Additionally, we quantified the number and type of skeletal muscle defects observed in the akirin,+/+,MTA-Like double heterozygous mutant embryos.