Loss of zebrafish dcst2 expression is not associated with muscle abnormalities

Abstract

In this study we examined if the gene encoding Dendritic Cell-specific Six Transmembrane domain containing protein 2 (dcst2) plays a role in vertebrate muscle biology. Using the CRISPR/Cas9 mutagenic system we generated a 2 nucleotide deletion in exon 3 of the zebrafish ortholog dcst2 which resulted in a premature stop codon. Homozygous carriers of the mutation displayed reduced transcriptional expression of dcst2 suggesting that our mutation was indeed disrupting gene function. Mutant dcst2 zebrafish developed normally to adulthood and displayed no differences in motor function using a free-swim and swim tunnel assays. Furthermore, histological examination of muscle cells revealed no differences in slow-twitch or fast-twitch muscle cell cross-sectional area in our mutants. We did observe that dcst2-/- zebrafish were slightly heavier in weight and males were infertile. The data collected here, suggest that dcst2 does not play a role in zebrafish muscle cell biology.