Published January 1, 2021
| Version v1
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Knockout of zebrafish desmin genes does not cause skeletal muscle degeneration but alters calcium flux
Creators
- 1. Hacettepe Univ, Dept Med Biol, Fac Med, TR-06100 Ankara, Turkey
- 2. Hacettepe Univ, Dept Biophys, Fac Med, TR-06100 Ankara, Turkey
- 3. Hacettepe Univ, Dept Stem Cell Sci, Grad Sch Hlth Sci, TR-06100 Ankara, Turkey
- 4. Hacettepe Univ, Dept Elect & Elect Engn, Fac Engn, TR-06800 Ankara, Turkey
- 5. Hacettepe Univ, Dept Histol & Embryol, Fac Med, TR-06100 Ankara, Turkey
- 6. Hacettepe Univ, Dept Pediat, Pathol Unit, Fac Med, TR-06100 Ankara, Turkey
- 7. Kings Coll London, Randall Ctr Cell & Mol Biophys, New Hunts House,Guys Campus, London SE1 1UL, England
Description
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.
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