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Open Access Research article

The salmonid myostatin gene family: a novel model for investigating mechanisms that influence duplicate gene fate

Casey B Lawson13, Takumu Niino13, Russell A Hermansen4, Vera Brok-Volchanskaya4, Melissa F Jackson23, Dilip K Garikipati13, David A Liberles4* and Buel D Rodgers123*

Author Affiliations

1 Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA

2 School of Molecular Biosciences, Washington State University, Pullman, WA, 99164, USA

3 Washington Center for Muscle Biology, Washington State University, Pullman, WA, 9916, USA

4 Department of Molecular Biology, University of Wyoming, Laramie, WY 82071, USA

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BMC Evolutionary Biology 2012, 12:202  doi:10.1186/1471-2148-12-202

Published: 8 October 2012

Abstract

Background

Most fishes possess two paralogs for myostatin, a muscle growth inhibitor, while salmonids are presumed to have four: mstn1a, mstn1b, mstn2a and mstn2b, a pseudogene. The mechanisms responsible for preserving these duplicates as well as the depth of mstn2b nonfunctionalization within the family remain unknown. We therefore characterized several genomic clones in order to better define species and gene phylogenies.

Results

Gene organization and sequence conservation was particularly evident among paralog groupings and within salmonid subfamilies. All mstn2b sequences included in-frame stop codons, confirming its nonfunctionalization across taxa, although the indels and polymorphisms responsible often differed. For example, the specific indels within the Onchorhynchus tshawytscha and O. nerka genes were remarkably similar and differed equally from other mstn2b orthologs. A phylogenetic analysis weakly established a mstn2b clade including only these species, which coupled with a shared 51 base pair deletion might suggest a history involving hybridization or a shared phylogenetic history. Furthermore, mstn2 introns all lacked conserved splice site motifs, suggesting that the tissue-specific processing of mstn2a transcripts, but not those of mstn2b, is due to alternative cis regulation and is likely a common feature in salmonids. It also suggests that limited transcript processing may have contributed to mstn2b nonfunctionalization.

Conclusions

Previous studies revealed divergence within gene promoters while the current studies provide evidence for relaxed or positive selection in some coding sequence lineages. These results together suggest that the salmonid myostatin gene family is a novel resource for investigating mechanisms that regulate duplicate gene fate as paralog specific differences in gene expression, transcript processing and protein structure are all suggestive of active divergence.

Keywords:
Salmon; Myostatin; Gene duplication; Subfunctionalization