Submission Type
Poster
Abstract
Zebrafish possess the ability to regenerate body parts such as the heart, fins, pancreas, brain, spinal cord, kidneys, and retina. When zebrafish retinal damage occurs, Müller glia divide and create neuronal precursor cells, which go on to become replacement retinal neurons. This allows zebrafish to recover from retinal damage. However, mutant zebrafish cannot fully develop and regenerate retinal cells. In particular, the good effort (gef) mutant allele of the chaf1b gene is characterized by a period of normal development, followed by cell death in highly proliferative developing tissues, including the retina, brain, and pectoral fins. The gef mutant retinal cells appear unaffected until roughly two days post-fertilization. This suggests a requirement for Chaf1b at the switch from cycling retinal progenitor cells to post-mitotic differentiating cells. It is proposed that Chaf1b mutations are not immediately lethal due to maternal deposition of functional proteins in the egg. Chaf1b is a subunit of the chromatin assembly factor (CAF1) complex, which is responsible for the assembly of histones at the replication fork during S phase. The location of Chaf1b protein has not been rigorously tested. We are testing antibodies generated against Chaf1b in gef-mutant embryo and wild-type embryo lysates to determine whether maternally provided Chaf1b persists differentially in later embryonic cells.
Recommended Citation
Welsch, Stephen; Coffee, Dan; Gilly, Zachary; Noe, Thadar; and Gibeault, Olivia, "179 - Chromosome Assembly Factor 1b in Zebrafish Retinal Development" (2025). GREAT Day Posters. 46.
https://knightscholar.geneseo.edu/great-day-symposium/great-day-2025/posters-2025/46
179 - Chromosome Assembly Factor 1b in Zebrafish Retinal Development
Zebrafish possess the ability to regenerate body parts such as the heart, fins, pancreas, brain, spinal cord, kidneys, and retina. When zebrafish retinal damage occurs, Müller glia divide and create neuronal precursor cells, which go on to become replacement retinal neurons. This allows zebrafish to recover from retinal damage. However, mutant zebrafish cannot fully develop and regenerate retinal cells. In particular, the good effort (gef) mutant allele of the chaf1b gene is characterized by a period of normal development, followed by cell death in highly proliferative developing tissues, including the retina, brain, and pectoral fins. The gef mutant retinal cells appear unaffected until roughly two days post-fertilization. This suggests a requirement for Chaf1b at the switch from cycling retinal progenitor cells to post-mitotic differentiating cells. It is proposed that Chaf1b mutations are not immediately lethal due to maternal deposition of functional proteins in the egg. Chaf1b is a subunit of the chromatin assembly factor (CAF1) complex, which is responsible for the assembly of histones at the replication fork during S phase. The location of Chaf1b protein has not been rigorously tested. We are testing antibodies generated against Chaf1b in gef-mutant embryo and wild-type embryo lysates to determine whether maternally provided Chaf1b persists differentially in later embryonic cells.
Comments
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