1st mouse by parthenogenesis?
Single gene knockout in dual maternal oocyte results in viable mice, but
some doubt study
By Cathy Holding

A study published in the advance online publication of Nature today (April
21) reports the first mouse created by parthenogenesis. But a leading
researcher called the results very confusing, saying they raise more
questions than answers.

Tomohiro Kono and colleagues from the Tokyo University of Agriculture,
Japan, report that they knocked out one allele of H19-a maternally expressed
gene thought to function as A noncoding mRNA that blocks IN CIS the
expression of Igf2-in an oocyte derived solely from two maternal genomes. A
normally developed and viable parthenote resulted, suggesting a pivotal role
for the paternally imprinted H19 gene in allowing Igf2 expression from the
paternal allele and controlling the requirement for a paternal genome,
according to the authors.

"When you put these two sets of chromosomes together functionally, the
individual would have a father-like genome with the original mother genome,
and therefore it works and gives rise to a live offspring," Patrick Tam,
head of the embryology unit at the Children's Medical Research Institute,
Westmead, Australia, who wrote an accompanying News and Views article, told
The Scientist.

In prior experiments, the Tokyo group had used a maternally imprinted genome
and a neutral genome, which still proved to be lethal, according to Wolf
Reik, head of developmental genetics and imprinting at the Babraham
Institute in Cambridge, UK. "What they are trying to do now is convert the
neutral genome into a paternal one by giving it this H19 deletion allele,
which allows the neutral genome to express Igf2-and this is clearly a key
event that needs to happen here," said Reik, who was not involved in the
study.

But Rudolf Jaenisch, professor of biology at the Whitehead Institute and the
Massachusetts Institute of Technology, Cambridge, US, found the paper flawed
and confusing. "I really know this literature," he told The
Scientist. "Igf2
mutations-total knockout, no Igf2 whatsoever-gives you live mice and every
mouse survives: they're all small." This suggests that expression of Igf2 is
not an absolute requirement for normal embryonic development, according to
Jaenisch, in contrast to the paper's results.

Read the rest at The Scientist dot com
http://www.biomedcentral.com/news/20040421/01

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