Abstract
Somatic cell nuclear transfer (SCNT), commonly referred to as cloning, results in the generation of offspring that, except for mitochondrial DNA, are genetically identical to the nuclear donor. We previously used a genetically modified bovine cell line as the donor for SCNT and obtained a calf, named Daisy, that was born without a tail. To determine whether the missing tail was a result of the genetic modification, we performed recloning experiments by using either cells from a sacrificed pregnancy of a second clone (Daisy's “twin” clone) or cells from tailless Daisy as donors for SCNT. Cloned fetuses from aborted pregnancies and a cloned live calf that died shortly after birth were examined and confirmed to all possess tails. Hence, the observed phenotype of Daisy's lacking tail is not due to the introduced transgene or a mutation present in the cell that was used for her production. Rather, the missing tail has most likely arisen from an epigenetic reprogramming error during development.
Highlights
Taillessness in cattle is a rare congenital defect
Results of a brief study of 50 tailless cows by Gilmore and Fechheimer (1957) suggest that taillessness in cattle is neither a simple dominant nor a simple recessive trait, an assumption that was inferred from test matings of tailless animals (Greene et al, 1973)
We show that recloning of a tailless transgenic calf yields fetuses and a live calf with tails, which suggests that the originally observed taillessness is not of genetic origin
Summary
Taillessness (anury) in cattle is a rare congenital defect. Statistical analysis of a study with 25 tailless animals of different breeds suggested an occurrence of between one in 3000 and one in 20,500 (Huston and Wearden, 1958). Results of a brief study of 50 tailless cows by Gilmore and Fechheimer (1957) suggest that taillessness in cattle is neither a simple dominant nor a simple recessive trait, an assumption that was inferred from test matings of tailless animals (Greene et al, 1973) This apparent lack of heritability contrasts with taillessness in Manx cats that is inherited through a dominant and homozygous lethal allele of the Manx M gene (Robinson, 1993) or in a reported mutated house mouse strain where a tailless phenotype was transmitted through two dominant and homozygous lethal alleles (Chesley and Dunn, 1936). A case of taillessness was reported in the highly inbred herd of Chillingham
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