Transgenic overexpression of follistatin 2 in blunt snout bream results in increased muscle mass caused by hypertrophy.

As a competitive binding protein, follistatin (FST) antagonizes myostatin (MSTN) function and promotes muscle growth. Overexpression of FST in transgenic mice results in dramatically increased muscle mass caused by hyperplasia and/or hypertrophy. Previously, we identified two functional divergent fst genes (gc fst1 and gc fst2 ) in grass carp ( Ctenopharyngodon idella ). The objectives of this study were to determine if gc fst genes have similar roles on promoting muscle growth in fish. We generated a heterozygous gc fst1 - and gc fst2 -transgenic F0 generation in blunt snout bream ( Megalobrama amblycephala ). We then produced a homozygous gynogenetic F1 generation, and eventually a homozygous transgenic F2 generation. Driven by the zebrafish skeletal muscle-specific gene Mylz2 promoter, high levels of gc fst1 or gc fst2 mRNAs were expressed in embryonic somites and adult muscles in homozygous gc fst1 - or gc fst2 -transgenic F2 blunt snout bream, respectively. In contrast to gc fst1 -transgenic fish or wild-type controls, adult gc fst2 -transgenic F2 blunt snout bream exhibited a double-muscling phenotype and marked increases in body height and thickness. Overexpression of gcfst2 caused significant fiber size enlargement in skeletal muscle in gc fst2 -transgenic F2 blunt snout bream. Our findings suggest that enhanced muscle growth induced by gcfst2 overexpression in transgenic blunt snout bream is caused by hypertrophic muscle growth. This approach may be used to promote directional breeding in important aquaculture species such as blunt snout bream in the future. Statement of relevance To promote directional breeding in important aquaculture species blunt snout bream, our research papers presents novel data on fish breeding. Our article complies with the Policy Statement for submission of manuscripts to the Genetics Section. [ABSTRACT FROM AUTHOR]