Placenta

These results [in mice] led to an extraordinary conclusion. Paternal genes, inherited from the
father, are responsible for making the placenta maternal genes, inherited from the mother,
are responsible for making the greater part of the embryo, especially its head and brain
[David Haig] had begun to reinterpret the mammalian placenta, not as a maternal organ
designed to give sustenance to the foetus, but more as a foetal organ desgined to parasitise the
maternal blood supply and brook no opposition in the process. He noted that the placenta
literally bores its way into the mothers vessels, forcing them to dilate, and then proceeds to
produce hormones which raise the mothers blood pressure and blood sugar. The mother
responds by raising her insulin levels to combat this invasion, yet, if for some reason the foetal
hormone is missing, the mother does not need to raise her insulin levels and a normal
pregnancy ensues. In other words, although mother and foetus have a common purpose, they
argue fiercely about the details of how much of the mothers resources the foetus may have exactly as they will later during weaning. But the foetus is built partly with maternal genes, so
it would not be surprising if these genes found themselves with, as it were, a conflict of
interest. The fathers genes in the foetus have no such worries. They do not have the mothers
interest at heart, except insofar as she provides a home for them. The fathers genes do not
trust the mothers genes to make a sufficiently invasive placenta; so they do the job
themselves. Modern evolutionary theorists, led by David Haig, now think of the placenta as
more like a parasitic takeover of the mothers body by paternal genes in the foetus. The
placenta tries, against maternal resistance, to control her blood-sugar levels and blood
pressure to the benefit of the foetus. Matt Ridley, Genome: The Autobiography of a
Species in 23 Chapters, Fourth Estate, 2000
In recent years, too, biologists have discovered a phenomenon called genomic imprinting,
which says that a gene inherited from the mother may behave differently from the same gene
inherited from the father. The Second Creation, Headline, 2001
Scientists have discovered a gene that plays a crucial role in the survival of female embryos.
The breakthrough provides valuable information about the way genes are regulated in the
developing embryo. It should also help improve the understanding of foetal loss, tumour
development, birth defects and mental retardation. The scientists, from the University of North
Carolina at Chapel Hill, carried out their research on female mice embryos. They examined a
gene called eed, which when functioning normally keeps the X chromosome inherited from the
father inactive, and many of its genes shut down in early placental cells. They discovered that
female embryos without a functioning eed do not survive because they cannot form a placenta.
Other studies have shown that the gene Xist is responsible for putting the molecular brakes

only on the X chromosome. As female mammals have two X chromosomes (XX) and males an
X and Y (XY), imbalance occurs because female embryos have twice as many X-linked genes.
That is where Xist comes into play. It gets turned on early in the development of the female
embryo. This gene is activated from the X chromosome that is going to be shut down - which in
early placental material is only the X from the father. Once the paternal X chromosome is shut
down, then the cells must continue to divide and keep it shut down. The new research has
found that it is the eed gene which performs this function. Lead researcher Dr Terry Magnuson
said: "Without eed functioning normally, the father's X chromosome is shut down and then it
comes back on. When that happens, too many X chromosome genes are active, there are
problems forming placental tissue, and female embryos die." The researchers also discovered
that a partially-functioning eed gene can lead to the development of leukaemia, skeletal
abnormalities and other problems. The gene also plays a vital role in telling cells where to go
in the developing embryo. Without this gene functioning in the proper way, those cells move to
the wrong place. And that can result in birth defects. BBC News, 2001
The embryos with an all-paternal genome develop a fine placenta, but no proper embryo;
while those with an all-maternal genome begin by making a good-looking embryo, but only a
poor placenta. For this reason parthenogenesis in mammals development of a whole new
animal from an unfertilised egg really does seem biologically impossible in mammals, even
though it is common enough in other animals, including many other vertebrates. In the
absence of divine intervention, virgin birth for mammals is not an option. Ian Wilmut and
Keith Campbell, Mammals Cloned, The Second Creation, 2001