Submission Type
Poster
Start Date
4-26-2023
Abstract
Chromatin assembly factor-1b (Caf-1b), one of the subunits of Chromatin assembly factor-1, is integral for retina differentiation in both humans and zebrafish. Fisher et. al found that apoptosis was stimulated in cells that lack Caf-1b at the S-phase check point by the tumor suppressor p53 as cells that lacked Caf-1b had a much higher expression of p53 then cells that contained Caf-1b. Fisher et. al proposed the model that Caf-1b is an inhibitor of p53 which stimulates apoptosis in the absence of Caf-1b (2007). However, it is not known what occurs when both Caf-1b and p53 are both removed. If we were to remove both Caf-1b and p53, we would expect that apoptosis would not occur in the embryo if the Fisher model were to be correct since although Caf-1b is not present, there is no p53 to stimulate apoptosis. We will accomplish this goal by using good effort mutants that lack Caf-1b and tp53/zdf1 mutants that lack p53; we will cross section mutants that are both good effort and tp53/zdf1 to compare the amount of apoptosis, as labeled with TUNEL staining, with cross sectioned good effort mutants. The good effort mutants will act as our positive control as apoptosis will be stimulated by p53 while the mutants that express both good effort and tp53/zdf1 will act as our experimental group.
Recommended Citation
Stephens, Noé; Brahmbhatt, Dhavan; Reitano-stayer, Isabel; and Haws, Hannah, "162 - The Importance of Chaf-1b and p53 in Zebrafish Apoptosis" (2023). GREAT Day Posters. 27.
https://knightscholar.geneseo.edu/great-day-symposium/great-day-2023/posters-2023/27
Included in
162 - The Importance of Chaf-1b and p53 in Zebrafish Apoptosis
Chromatin assembly factor-1b (Caf-1b), one of the subunits of Chromatin assembly factor-1, is integral for retina differentiation in both humans and zebrafish. Fisher et. al found that apoptosis was stimulated in cells that lack Caf-1b at the S-phase check point by the tumor suppressor p53 as cells that lacked Caf-1b had a much higher expression of p53 then cells that contained Caf-1b. Fisher et. al proposed the model that Caf-1b is an inhibitor of p53 which stimulates apoptosis in the absence of Caf-1b (2007). However, it is not known what occurs when both Caf-1b and p53 are both removed. If we were to remove both Caf-1b and p53, we would expect that apoptosis would not occur in the embryo if the Fisher model were to be correct since although Caf-1b is not present, there is no p53 to stimulate apoptosis. We will accomplish this goal by using good effort mutants that lack Caf-1b and tp53/zdf1 mutants that lack p53; we will cross section mutants that are both good effort and tp53/zdf1 to compare the amount of apoptosis, as labeled with TUNEL staining, with cross sectioned good effort mutants. The good effort mutants will act as our positive control as apoptosis will be stimulated by p53 while the mutants that express both good effort and tp53/zdf1 will act as our experimental group.
Comments
Sponsored by Travis Bailey