Knockout of zebrafish desmin genes does not cause skeletal muscle degeneration but alters calcium flux

Gülsüm Kayman Kürekçi, Ecem Kural Mangit, Cansu Koyunlar, Seyda Unsal, Berk Saglam, Bora Ergin, Merve Gizer, Ismail Uyanik, Niloufar Boustanabadimaralan Düz, Petek Korkusuz, Beril Talim, Nuhan Purali, Simon M. Hughes, Pervin R. Dincer*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

17 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number7505
JournalScientific Reports
Volume11
Issue number1
DOIs
Publication statusPublished - 5 Apr 2021

Bibliographical note

Funding Information:
This work was supported by The Scientific and Technological Research Council of Turkey, Project No. 214S174 to P.R.D. S.M.H. is an MRC Scientist with MRC Programme Grant G1001029 and MR/N021231/1 support.

Publisher Copyright:
© 2021, The Author(s).

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