TitleSarcolipin Exhibits Abundant RNA Transcription and Minimal Protein Expression in Horse Gluteal Muscle.
Publication TypeJournal Article
Year of Publication2020
AuthorsAutry, JM, Karim, CB, Perumbakkam, S, Finno, CJ, McKenzie, EC, Thomas, DD, Valberg, SJ
JournalVet Sci
Date Published2020 Nov 13

Ca regulation in equine muscle is important for horse performance, yet little is known about this species-specific regulation. We reported recently that horse encode unique gene and protein sequences for the sarcoplasmic reticulum (SR) Ca-transporting ATPase (SERCA) and the regulatory subunit sarcolipin (SLN). Here we quantified gene transcription and protein expression of SERCA and its inhibitory peptides in horse gluteus, as compared to commonly-studied rabbit skeletal muscle. RNA sequencing and protein immunoblotting determined that horse gluteus expresses the gene (SERCA1) as the predominant SR Ca-ATPase isoform and the gene as the most-abundant SERCA inhibitory peptide, as also found in rabbit skeletal muscle. Equine muscle expresses an insignificant level of phospholamban (PLN), another key SERCA inhibitory peptide expressed commonly in a variety of mammalian striated muscles. Surprisingly in horse, the RNA transcript ratio of -to- is an order of magnitude than in rabbit, while the corresponding protein expression ratio is an order of magnitude than in rabbit. Thus, is not efficiently translated or maintained as a stable protein in horse muscle, suggesting a non-coding role for supra-abundant mRNA. We propose that the lack of SLN and PLN inhibition of SERCA activity in equine muscle is an evolutionary adaptation that potentiates Ca cycling and muscle contractility in a prey species domestically selected for speed.

Alternate JournalVet Sci
PubMed ID33202832
PubMed Central IDPMC7711957
Grant ListHL139065 / NH / NIH HHS / United States
GM27906 / NH / NIH HHS / United States
R01 HL139065 / HL / NHLBI NIH HHS / United States
D16EQ-004 / / Morris Animal Foundation /
D14EQ-021 / / Morris Animal Foundation /
AG26160 / NH / NIH HHS / United States
R01 AG026160 / AG / NIA NIH HHS / United States