The oocyte contains many more mitochondria and than does a somatic cell and it has been predicted that most of the mitochondria in cloned animals would have originated from the egg, but the inability to detact any mitochondrial DNA from the donor cells was a surprise. None of the mitochondria from the sperm survive after normal fertilisation and there may be specific mechanisms that favour oocyte mitochondria during early development. One of the limitations to large scale 'reprogramming' of human cells by nuclear transfer is the limited supply of human eggs. One group in the US, Advanced Cell Technologies, has claimed some success in transferring human cells to bovine oocytes as a way round this bottleneck. The results of the present study, however suggest that any cells derived from such 'embryos' would be populated by bovine mitochondria and therefore unlikely to be viable in the longer term.
Enteric diseases are a common cause of death in young pigs.
Maternal antobodies provide some protection as does caccination of the pigglets themselves but our recent studies in mice have shown that it is now becoming practical to consider transgenic alternatives to these conventional approaches. Using our expertise in targeting transgene expression in the mammary gland, we have successfully expressed two specific monoclonal antibodies in mouse milk. In collaboration with Dr Adreas Kolb of the Hannah Research Institute and Dr Stanley Perlman of the University of Iowa, we have expressed, again in mouse milk, a monoclonal antibody to mouse hepatitis virus. This latter target is important because it will allow us to challenge the offpsring of such transgenic animals with the mouse virus and test if the antibodies really do provide protection. Expression of transgenes is, however, frequently confounded by unpredictable effects of site of integration and copy number.