PUBLICATION
Manipulation of Proteostasis Networks in Transgenic ZAAT Zebrafish via CRISPR-Cas9 Gene Editing
- Authors
- Fung, C., Miles, L.B., Bryson-Richardson, R.J., Bird, P.I.
- ID
- ZDB-PUB-231219-3
- Date
- 2024
- Source
- Methods in molecular biology (Clifton, N.J.) 2750: 193219-32 (Other)
- Registered Authors
- Bird, Phillip I., Bryson-Richardson, Robert, Fung, Connie
- Keywords
- AATD, Atf6a, CRISPR–Cas9, Man1b1, Zebrafish, α1-antitrypsin
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- CRISPR-Cas Systems/genetics
- Gene Editing
- Humans
- Mice
- Perciformes*
- Proteostasis*/genetics
- Zebrafish/genetics
- PubMed
- 38108964 Full text @ Meth. Mol. Biol.
Citation
Fung, C., Miles, L.B., Bryson-Richardson, R.J., Bird, P.I. (2024) Manipulation of Proteostasis Networks in Transgenic ZAAT Zebrafish via CRISPR-Cas9 Gene Editing. Methods in molecular biology (Clifton, N.J.). 2750:193219-32.
Abstract
The CRISPR-Cas9 genome editing system is used to induce mutations in genes of interest resulting in the loss of functional protein. A transgenic zebrafish α1-antitrypsin deficiency (AATD) model displays an unusual phenotype, in that it lacks the hepatic accumulation of the misfolding Z α1-antitrypsin (ZAAT) evident in human and mouse models. Here we describe the application of the CRISPR-Cas9 system to generate mutant zebrafish with defects in key proteostasis networks likely to be involved in the hepatic processing of ZAAT in this model. We describe the targeting of the atf6a and man1b1 genes as examples.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping