Myostatin expression in porcine tissues: tissue specificity and developmental and postnatal regulation

Abstract

The objective of this study was to establish the developmental pattern and tissue specificity of porcine myostatin expression and to evaluate expression in skeletal muscle during circumstances in which muscle growth was altered. Northern blot analysis revealed two transcripts (1.5 and 0.8 kb). Myostatin mRNA was detected in whole fetuses at 21 and 35 days and was markedly increased ( P < 0.05) by 49 days. At birth, mRNA abundance in longissimus muscle had declined significantly ( P < 0.05) from that at day 105 of gestation and continued to decrease ( P < 0.05) to its lowest level 2 wk postnatally (4 kg body wt). Myostatin expression was higher ( P < 0.05) at 55, 107, and 162 kg body wt than at 4 kg body wt. Postnatally, myostatin mRNA was detected in skeletal muscle and mammary gland. Expression at birth was 65% higher ( P < 0.04) in longissimus muscle of low-birth-weight piglets (0.57 ± 0.052 kg body wt) vs. normal (1.37 ± 0.077 kg body wt) littermates, irrespective of gender. However, suppression of longissimus muscle growth by food deprivation (3 days) did not alter ( P > 0.15) myostatin expression in either 4- or 7-wk-old piglets. Additionally, myostatin mRNA abundance was not changed by porcine growth hormone administration in growing animals. These data indicate that myostatin expression in skeletal muscle peaks prenatally and that greater expression is associated with low birth weight. Expression in mammary gland indicates a possible role for myostatin in mammary gland development and/or lactation.

Key signalling factors and pathways in the molecular determination of skeletal muscle phenotype

“…A point mutation that changes the cysteine residue in Mst to a tyrosine (Kambadur et al, 1997). The porcine Mst gene has been molecularly cloned and characterised, but a mutation that confers the enlarged muscle phenotype has not been described (Ji et al, 1998). Mst arrests muscle cells in the G 1 and G 2 phases of the cell cycle, through the up-regulation of cyclin-dependent kinase (cdk) inhibitor p21 and down-regulation of cdk-2, thereby inhibiting cell proliferation (Thomas et al, 2000).…”

Resistance to body fat gain in ‘double-muscled’ mice fed a high-fat diet

“…Whole-embryo in situ hybridization shows that myostatin is first expressed in mouse embryos in the myotome compartment of somites, and myostatin transcripts can still be detected in adult skeletal muscle. 1,2 Myostatin is a negative regulator of skeletal muscle growth, and myostatin null mice have approximately twice the skeletal muscle mass of normal mice. 1 Studies of mice lacking myostatin indicate that myostatin knockout mice do not accumulate as much body fat during growth and maturation as normal mice, so that 'double-muscled' adult knockout mice tend to be similar in mass to normal adult mice.…”

MicroRNA-27a promotes porcine myoblast proliferation by downregulating myostatin expression

“…The complete CDS of myostatin has been cloned from swine (Ji et al, 1998), cattle (Grobet et al, 1997), horse (Hosoyama et al, 2002) and sheep (Sharma et al, 1999). MiRNAs negatively regulate gene expression at the posttranscriptional level via binding to the 3'UTR of target mRNAs (Bartel, 2004;Tanzer and Stadler, 2004;de Moor et al, 2005;Gladka et al, 2012).…”