Cloning for transplant may produce fatal genetic imbalances

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The Independent Online

Plans to clone human embryos to generate vital stem cells for transplant operations are likely to fail using the techniques currently available, a study has found.

Plans to clone human embryos to generate vital stem cells for transplant operations are likely to fail using the techniques currently available, a study has found.

Scientists at the University of Connecticut have discovered that cloning produces genetic imbalances, which could explain why so many cloned animals are stillborn or suffer from medical problems after birth and die prematurely. The same flaws could also jeopardise the use of stem cells derived from cloned human embryos produced for "therapeutic" purposes. The resulting tissues would be too defective to repair damaged organs, the scientists said.

"Currently, cloning technology is immature and shouldn't be expanded out to humans," said Cindy Tian, assistant professor of developmental biology. "It's bad news at the moment for therapeutic cloning but it's good news in that we're realising what needs to be overcome," she said.

The study, published in the journal Nature Genetics, examined 10 genes on the X chromosomes of 10 cloned female calves, six of which had died either in the womb or soon after birth.

They looked at a process called X-chromosome inactivation. This normally results in one of the two X chromosomes of females being switched off so that the cells of females have the same number of genes switched on as males, who have only one X chromosome.

The scientists found that nine out of 10 genes for the dead clones were abnormal in the way they were activated, or "expressed". They also found that this pattern of activation differed from one cloned animal to another, indicating the random nature of the process.

There were no such abnormalities in gene activation in the clones that had lived and in female calves resulting from normal sexual reproduction.

During normal animal development only the X chromosome inherited from the mother is activated in the placenta, but the study showed that both X chromosomes were active in the placentas of the dead cows. This might explain why the placentas of cloned animals are often bigger than normal and why some cloned foetuses are abnormally large.

Jerry Yang, who led the Connecticut team, said the work could explain why some 80 per cent of cloned animals died during pregnancy or soon after birth.

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