Looking at the Interaction Between the Proteins Akirin and MTA-Like for Cardiac and Skeletal Muscle Development
Disciplines
Cell and Developmental Biology | Molecular Genetics
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 can range from minor to severe, with some of the most severe cases being deformed or missing heart valves. Though we know this developmental issue is linked to genetics, the specific genes that are responsible for the cardiac defect remains unknown. To better understand the genetic mechanism(s) behind heart development, the Nowak lab has identified an acute number of genetic markers that have an impactful role in developing an embryonic heart. To simplify the process the Nowak lab uses Drosophila (aka the fruit fly) to be used as a model organism to better understand and analyze heart development. There are many aspects of development that are conserved between Drosophila and humans. With this notion, we can use these similarities to understand the genetics behind human heart development.
We previously identified the conserved nuclear protein Akirin to be an important regulator of gene expression for cardiac development. Our data suggests Akirin works with the Nucleosome Remodeling and Deacetylase (NuRD) complex for proper heart development. Since NuRD contains more than ten different subunits, a variation in mutations within the complex can lead to a variety of abnormalities, including abnormal muscle patterns, misshapen hearts, and/or decrease in cardiomyoblasts. For the purposes of my project, the NuRD subunit MTA-Like will be examined and how it plays a critical role in cardiac development and cardiac function. To achieve this goal recombination of the MTA-Like and toll-cGFP genes are being used to produce possible heterozygous embryonic mutations. To properly analyze these mutations live confocal imaging will be used to record and analyze heartbeats that are produced from the recombination of the MTA-Like and Akirin cross. The cGFP protein will place several markers on the muscles that we wish to analyze.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Scott Nowak
Looking at the Interaction Between the Proteins Akirin and MTA-Like 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 can range from minor to severe, with some of the most severe cases being deformed or missing heart valves. Though we know this developmental issue is linked to genetics, the specific genes that are responsible for the cardiac defect remains unknown. To better understand the genetic mechanism(s) behind heart development, the Nowak lab has identified an acute number of genetic markers that have an impactful role in developing an embryonic heart. To simplify the process the Nowak lab uses Drosophila (aka the fruit fly) to be used as a model organism to better understand and analyze heart development. There are many aspects of development that are conserved between Drosophila and humans. With this notion, we can use these similarities to understand the genetics behind human heart development.
We previously identified the conserved nuclear protein Akirin to be an important regulator of gene expression for cardiac development. Our data suggests Akirin works with the Nucleosome Remodeling and Deacetylase (NuRD) complex for proper heart development. Since NuRD contains more than ten different subunits, a variation in mutations within the complex can lead to a variety of abnormalities, including abnormal muscle patterns, misshapen hearts, and/or decrease in cardiomyoblasts. For the purposes of my project, the NuRD subunit MTA-Like will be examined and how it plays a critical role in cardiac development and cardiac function. To achieve this goal recombination of the MTA-Like and toll-cGFP genes are being used to produce possible heterozygous embryonic mutations. To properly analyze these mutations live confocal imaging will be used to record and analyze heartbeats that are produced from the recombination of the MTA-Like and Akirin cross. The cGFP protein will place several markers on the muscles that we wish to analyze.