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updated 4/28/2004 6:27:52 PM ET 2004-04-28T22:27:52

If research in mice holds true, men -- and hence, their manly services -- may no longer be needed.

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At least that's the indication of a new study boasting a scientific first: Mice that reached adulthood through parthenogenesis, a form of reproduction in which the female egg develops into a live birth without male fertilization.

Parthenogenesis, from the Greek word for "virgin birth," is old hat for egg-laying species such as insects, fish, and lizards. With these species, which ironically includes some birds and bees (the very symbol for the more traditional way of making babies), females produce eggs, but they develop without any help or need of would-be fathers.

Yet no mammal has ever been known to give birth through parthenogenesis, and previous mice, monkeys, and human embryos created this way have never survived for more than a few days. One major reason: In mammals fathers remain a necessity. Without the genetic material from sperm the placenta develops poorly and the embryo cannot survive. The placenta provides oxygen and nutrients to developing embryos.

Does this suggest that other male mammals -- namely, us -- will lose some of our baby-making value? Rest easy, guys, and don't shelve those Barry White tunes just yet.

"This is not going to be a straight-forward technique to enable parthenogenetic reproduction of a mammalian species," Australian embryologist Patrick Tam, Ph.D., tells WebMD. He says that the mice used in his study were not ordinary mice. These mice contained a specifically engineered gene that altered the activity of the other chromosomes.

Indeed. These mice developed from eggs that contained only maternal genetic material, unlike other mammals which develop through sexual reproduction and contain genetic material from both parents.

In the study the researchers combined chromosomes from cells with a missing key "male" gene -- called H19 -- with chromosomes from a fully grown egg which contains only maternal genes. In the past, embryos created this way died shortly before birth because of a poorly developed placenta. This time the researchers were able to create mice that developed normally and survived for much longer. One of the new pups was even able to reproduce after reaching adulthood. The report appears in this week's Nature.

"These findings provide the most compelling genetic evidence that it is absolutely essential to maintain some differences in the activity of genes from the father and the mother for the embryo to grow and develop," says Tam, who wrote an accompanying editorial in Nature but was not involved in the Japanese study. "This phenomenon is called 'genomic imprinting,' whereby the same gene may be marked differently for function depending on from which parent it is inherited."

That's important because it could lead to a better understanding about why some human pregnancies fail during the first trimester, says parthenogenesis expert Kent E. Vrana, Ph.D., of Penn State College of Medicine.

"What these researchers found is that in developing mice, parthenogenesis may typically fail at day 10, mid-gestation. But when they tweak the genes, they could get it to day 13. They tweak genes again and reach day 17, and tweak again and get the mice to full-term," he tells WebMD. Full-term pregnancy for mice is typically 19 to 31 days.

"This research is not going to provide a tool to create new clones or develop stem cell technologies, but it does provide new information on embryo development," says Vrana, who chairs the pharmacology department. "With better understand of how embryo development works, we could better understand how to correct it when it doesn't -- and better understand why some pregnancies fail early on."

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