Submission Title
Submission Type
Poster
Start Date
April 2020
Abstract
Zebrafish are a model organism for studying developmental abnormalities, especially in the eye. The good effort (gef) mutant zebrafish have smaller eyes than wild-type embryos due to rapid retinal degeneration that becomes apparent only after two days post fertilization. The genetic problem arises from a deletion of intronic DNA sequence which leads to the loss of an exon and disrupts the coding region of the Cha1b protein. Chaf1b is a subunit of the Chromosome assembly factor 1 (CAF-1), a complex of three proteins which has a role in histone loading and chromatin regulation. This small eye phenotype has been hypothesized to be due to Tp53-mediated apoptosis, however, phenotypic analysis from complex tp53-morphants or tp53zdf1 mutants and gef mutants suggests that the cause of cell death is not Tp53 dependent. Instead, we hypothesize that these issues are due to faulty signaling pathways, such as her4.1 and ascl1a. These specific signaling molecules are involved in retinal cell fate specification. Both of these molecules are under direct control of histone deacetylases which selectively regulate both genes during retinal development. Differences in her4.1 and ascl1a expression levels between gef and wild-type zebrafish embryos were analyzed by in situ hybridization.
Recommended Citation
Amato, Rico; Beiter, Tessa; and Lepore, Christopher, "155— Analysis of her4.1 and ascl1a in gef Mutants" (2020). GREAT Day Posters. 86.
https://knightscholar.geneseo.edu/great-day-symposium/great-day-2020/posters-2020/86
Included in
155— Analysis of her4.1 and ascl1a in gef Mutants
Zebrafish are a model organism for studying developmental abnormalities, especially in the eye. The good effort (gef) mutant zebrafish have smaller eyes than wild-type embryos due to rapid retinal degeneration that becomes apparent only after two days post fertilization. The genetic problem arises from a deletion of intronic DNA sequence which leads to the loss of an exon and disrupts the coding region of the Cha1b protein. Chaf1b is a subunit of the Chromosome assembly factor 1 (CAF-1), a complex of three proteins which has a role in histone loading and chromatin regulation. This small eye phenotype has been hypothesized to be due to Tp53-mediated apoptosis, however, phenotypic analysis from complex tp53-morphants or tp53zdf1 mutants and gef mutants suggests that the cause of cell death is not Tp53 dependent. Instead, we hypothesize that these issues are due to faulty signaling pathways, such as her4.1 and ascl1a. These specific signaling molecules are involved in retinal cell fate specification. Both of these molecules are under direct control of histone deacetylases which selectively regulate both genes during retinal development. Differences in her4.1 and ascl1a expression levels between gef and wild-type zebrafish embryos were analyzed by in situ hybridization.
Comments
Sponsored by Travis Bailey
This project was made possible by a generous TRAC grant from the Geneseo Foundation.