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Insertional vs Targeted Mutagenesis in the Development of Zebrafish as an In Vivo Model for Cardiomyopathy

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dc.contributor.advisor Dawson, John Ojehomon, Matiyo 2020-04-29T14:31:09Z 2020-04-29T14:31:09Z 2020-04-20 2020-04-09 2020-04-29
dc.description.abstract Heart failure is a global economic burden and can be caused by cardiomyopathy, a disease of the myocardium. Mutations in genes encoding sarcomere proteins have been known to cause cardiomyopathy. One of these sarcomere proteins is α-cardiac actin (ACTC), which is needed for proper contraction of the heart. To better understand how mutations in the ACTC protein cause cardiomyopathy, an in vivo model like zebrafish can be used to understand the molecular mechanism that occurs. Using transposons (insertional) or Clustered Regularly Interspaced Palindromic Repeats (CRISPRs) (targeted), zebrafish can be engineered to carry these mutations and the impact can be studied. The transposon system proved to be unstable as the inserted transposon underwent transcriptional repression. To use the CRISPR system, identifying which zfactc gene to target is necessary. Performing WMISH and RT-qPCR, zfacta1b seems to be the best candidate for targeted mutagenesis due to its early expression in the heart. en_US
dc.language.iso en en_US
dc.rights Attribution 4.0 International *
dc.rights.uri *
dc.subject Cardiomyopathy en_US
dc.subject cardiac actin en_US
dc.subject zebrafish en_US
dc.subject Transposons en_US
dc.subject CRISPRs en_US
dc.title Insertional vs Targeted Mutagenesis in the Development of Zebrafish as an In Vivo Model for Cardiomyopathy en_US
dc.type Thesis en_US Molecular and Cellular Biology en_US Master of Science en_US Department of Molecular and Cellular Biology en_US
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Attribution 4.0 International Except where otherwise noted, this item's license is described as Attribution 4.0 International