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Although the high failure rate has been attributed to incomplete reprogramming of the somatic nuclei during the cloning process, the exact cause is not fully known. To elucidate the cause of death in cloned offspring, 12 deceased offspring cloned by SCNT were necropsied. The clones were either stillborn just prior to delivery or died with dyspnea shortly after birth. On gross examination, defects in the anterior abdominal wall and increased heart and liver sizes were found. Notably, a significant increase in muscle mass and macroglossia lesions were observed in deceased SCNT\u2010cloned dogs. Interestingly, the expression of myostatin, a negative regulator of muscle growth during embryogenesis, was down\u2010regulated at the mRNA level in tongues and skeletal muscles of SCNT\u2010cloned dogs compared with a normal dog. Results of the present study suggest that decreased expression of myostatin in SCNT\u2010cloned dogs may be involved in morphological abnormalities such as increased muscle mass and macroglossia, which may contribute to impaired fetal development and poor survival rates. Mol. Reprod. Dev. 78:337\u2013346, 2011. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mrd.21309","type":"journal-article","created":{"date-parts":[[2011,4,25]],"date-time":"2011-04-25T17:37:17Z","timestamp":1303753037000},"page":"337-346","source":"Crossref","is-referenced-by-count":14,"title":["Morphological abnormalities, impaired fetal development and decrease in myostatin expression following somatic cell nuclear transfer in 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