Improving rainbow trout (Oncorhynchus mykiss) growth by treatment with a fish (Paralichthys olivaceus) myostatin prodomain expressed in soluble forms in E. coli

Strategies for enhancing skeletal muscle growth of aquaculture species are needed to meet the challenges of the increasing worldwide consumption of fish. One approach appears to be the inhibition of the activity of myostatin (MSTN), a member of the transforming growth factor-β superfamily that acts as a potent negative regulator of skeletal muscle growth. In mammalian vertebrates, MSTN activity is negatively regulated by MSTN prodomain, the N-terminal part of proMSTN cleaved during post-translational MSTN processing, but the role of MSTN prodomain on MSTN activity in fish is less clear. This study was designed to express a fish (Paralichthys olivaceus) MSTN-1 prodomain in soluble forms in E. coli, to examine its capacity to suppress MSTN activity in vitro, and to investigate the effect of treating fish with the MSTN-1 prodomain on fish growth. It was found that Rosetta-gami 2(DE3)pLysS strains transformed with pET32a or pMALc2x expression constructs carrying the P. olivaceus MSTN-1 prodomain (poMSTNpro) sequence could express soluble, cytoplasmic poMSTNpros. Affinity-purified poMSTNpros inhibited MSTN bioactivity in an in vitro reporter gene assay system. For the first time, it was observed that treating rainbow trout (Oncorhynchus mykiss) with either of the recombinant poMSTNpros improved the body mass growth of the fish up to 42% without affecting length growth. The results indicate that MSTN-1 prodomain suppresses MSTN activity in fish like it does in mammalian vertebrates. At the same time, the results demonstrate the potential of MSTN-based biotechnology to improve fish growth in aquaculture.