Knockout of zebrafish desmin genes does not cause skeletal muscle degeneration but alters calcium flux
- Kayman Kürekçi, G., Kural Mangit, E., Koyunlar, C., Unsal, S., Saglam, B., Ergin, B., Gizer, M., Uyanik, I., Boustanabadimaralan Düz, N., Korkusuz, P., Talim, B., Purali, N., Hughes, S.M., Dincer, P.R.
- Scientific Reports 11: 7505 (Journal)
- Registered Authors
- Hughes, Simon M.
- MeSH Terms
- Base Sequence
- Embryo, Nonmammalian/metabolism
- Gene Expression Profiling
- Gene Expression Regulation, Developmental
- Gene Knockout Techniques*
- Muscle Fibers, Skeletal/pathology
- Muscle, Skeletal/metabolism*
- Muscle, Skeletal/pathology*
- Muscle, Skeletal/ultrastructure
- Neuromuscular Junction/pathology
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- 33820917 Full text @ Sci. Rep.
Kayman Kürekçi, G., Kural Mangit, E., Koyunlar, C., Unsal, S., Saglam, B., Ergin, B., Gizer, M., Uyanik, I., Boustanabadimaralan Düz, N., Korkusuz, P., Talim, B., Purali, N., Hughes, S.M., Dincer, P.R. (2021) Knockout of zebrafish desmin genes does not cause skeletal muscle degeneration but alters calcium flux. Scientific Reports. 11:7505.
Desmin is a muscle-specific intermediate filament protein that has fundamental role in muscle structure and force transmission. Whereas human desmin protein is encoded by a single gene, two desmin paralogs (desma and desmb) exist in zebrafish. Desma and desmb show differential spatiotemporal expression during zebrafish embryonic and larval development, being similarly expressed in skeletal muscle until hatching, after which expression of desmb shifts to gut smooth muscle. We generated knockout (KO) mutant lines carrying loss-of-function mutations for each gene by using CRISPR/Cas9. Mutants are viable and fertile, and lack obvious skeletal muscle, heart or intestinal defects. In contrast to morphants, knockout of each gene did not cause any overt muscular phenotype, but did alter calcium flux in myofibres. These results point to a possible compensation mechanism in these mutant lines generated by targeting nonsense mutations to the first coding exon.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes