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
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