title: Phenotypic flexibility of skeletal muscle and heart masses and expression of myostatin and tolloid-like proteinases in migrating passerine birds.
abstract: Migrant birds require large flight muscles and hearts to enhance aerobic capacity and support sustained flight. A potential mechanism for increasing muscle and heart masses during migration in birds is the muscle growth inhibitor myostatin and its metalloproteinase activators, tolloid-like proteinases (TLL-1 and TLL-2). We hypothesized that myostatin, TLL-1 and TLL-2 are downregulated during migration in pectoralis and hearts of migratory passerines to promote hypertrophy. We measured seasonal variation of tissue masses, mRNA expression of myostatin, TLL-1, and TLL-2, and myostatin protein levels in pectoralis muscle and heart for yellow warblers (Setophaga petechia), warbling vireos (Vireo gilvus), and yellow-rumped warblers (Setophaga coronata). Pectoralis mass was greatest in spring for warbling vireos and yellow warblers, but was stable between spring and fall for yellow-rumped warblers. Heart mass was higher in spring than in fall for yellow-rumped warblers, lowest in fall for warbling vireos, and seasonally stable for yellow warblers. Pectoralis and heart mRNA expression of myostatin and the TLLs did not differ significantly for any of the three species, offering little support for our hypothesis for a prominent role for myostatin in regulating migration-induced variation in pectoralis and heart masses. In contrast, pectoralis myostatin protein levels were lowest in spring for all three species, consistent with our hypothesis. Myostatin protein levels in heart, however, were seasonally stable for warbling vireos and yellow warblers, and increased in spring relative to fall for yellow-rumped warblers. These data offer mixed support for our hypothesis for the pectoralis, but suggest that myostatin is not a prominent regulator of migration-induced heart hypertrophy. Moreover, the different seasonal patterns for pectoralis mRNA and protein expression suggest that post-transcriptional modification of myostatin may contribute to pectoralis mass regulation during migration.
authors.affiliation: Department of Biology, University of South Dakota, Vermillion, SD, 57069, USA.
authors.forename: Marisa O
authors.initials: MO
authors.lastname: King
authors.forename: Yufeng
authors.initials: Y
authors.lastname: Zhang
authors.forename: Travis
authors.initials: T
authors.lastname: Carter
authors.forename: Jake
authors.initials: J
authors.lastname: Johnson
authors.forename: Erin
authors.initials: E
authors.lastname: Harmon
authors.forename: David L
authors.initials: DL
authors.lastname: Swanson
mesh_terms: D000704:Analysis of Variance; D025041:Animal Migration / Q000502:physiology*; D000818:Animals; D015153:Blotting, Western; D005786:Gene Expression Regulation / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D055435:Myostatin / Q000378:metabolism*; D009929:Organ Size / Q000502:physiology; D046109:Passeriformes / Q000502:physiology*; D010369:Pectoralis Muscles / Q000502:physiology*; D060888:Real-Time Polymerase Chain Reaction; D012621:Seasons; D013023:South Dakota; D013045:Species Specificity; D055394:Tolloid-Like Metalloproteinases / Q000378:metabolism*
chemical_list: D055435:Myostatin; D055394:Tolloid-Like Metalloproteinases