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Few studies exist on homozygous myostatin gene mutant (MSTN−/−) pigs, especially on their reproductive ability. We have previously shown that semen quality of homozygous MSTN−/− boars is comparable to that of wild type (WT). However, no data exist on the reproductive ability of heterozygous MSTN gene mutant (MSTN+/−) sows. The present study highlights showed that the heterozygous MSTN+/− sows have delayed pubertal age than WT sows (255.80 ± 6.79 versus 191.10 ± 3.42, respectively). The number of services per pregnancy of heterozygous MSTN+/− sows is significantly higher than that of WT sows (3.33 ± 0.43 versus 1.60 ± 0.25, respectively). Moreover, although heterozygous MSTN+/− sows have natural reproduction ability, their litter size was significantly lower than that of WT sows (7.75 ± 0.44 versus 14.25 ± 0.60, respectively). Offsprings generated from heterozygous MSTN+/− sow and homozygous MSTN−/− boar were genotyped with the PCR and sequencing method to detect myostatin mutation and to identify whether the piglets are homozygous MSTN−/− or heterozygous MSTN+/−. The proportion of homozygous MSTN−/− piglets was significantly lower than that of heterozygous MSTN+/− piglets (2.50 ± 0.35 versus 5.25 ± 0.60, respectively). Furthermore, none of the sows presented dystocia, and the phenotype of heterozygous MSTN+/− piglets was normal. However, 10% homozygous MSTN−/− piglets died of dyspnoea within 2 hr after birth, 60% of homozygous MSTN−/− piglets showed large tongues, and 50% had umbilical hernias. In summary, this study for the first time reports the reproduction traits of heterozygous MSTN+/− sows crossbred with homozygous MSTN−/− boars. This study will pave the way in a new direction for the breeding and development of super lean meat varieties in the future.

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Herein, we investigate the high incidence of umbilical hernia and tippy-toe standing and their underlying changes in gene expression and proliferation in myostatin knockout (MSTN -/-) pigs. Thirtysix male MSTN -/pigs were generated by somatic cell nuclear transfer (SCNT). These pigs presented a considerably high incidence of tippy-toe standing and umbilical hernia (69.4% and 61.1%, respectively). The tendon to body weight ratio was significantly lower than wild-type pigs (0.202 ± 0.017 vs 0.250 ± 0.004, respectively). The crimp length of the MSTN -/tendon was significantly longer than that of wild-type pigs. The expression of MSTN and the activin type IIB (ACVR2B) was detected in the tendon and linea alba of MSTN -/pigs. MSTN treatment significantly increased the phosphorylation of Smad2/ 3 in both tendon and linea alba fibroblasts. Type I collagen (Col1A) and Scleraxis (Scx) expression levels in the tendon and linea alba of MSTN -/pigs were significantly lower than those in wild-type in vivo, whereas and cyclin-dependent kinase inhibitor 1 (p21) expression levels were higher. Treatment of tendon and linea alba fibroblasts with recombinant MSTN increased Col1A and Scx and decreased p21 expression in vivo. Moreover, there was a significant increase in fibroblast proliferation after treatment. The results indicated that MSTN regulates collagen expression and proliferation in tendon and linea alba fibroblasts; thus, MSTN deficiency causes collagenrelated pathological features in MSTN -/pigs. Hence, MSTN could be used as a therapeutic target for treating UH and tendon abnormalities.

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