Like a Virgin by Prasad, Aarathi (recommended reading txt) 📕

and sends the egg on the path of development, sometimes building remarkably well-developed organs and features. Their origin is inextricably linked to parthenogenesis, but how exactly is the egg triggered to start dividing without first being fertilized? To this question, certain mutant mice may hold the answer.

The structure of most cells in the body can be grossly divided into two areas: the nucleus and the cytoplasm. The nucleus can be thought of as the control centre of the cell. In the nucleus are the chromosomes, which carry the vast majority of the cell’s content of DNA, the all-important genetic instructions for the new being. The cytoplasm is a fluid matrix that surrounds the nucleus and all the other organelles, or miniature vital ‘organs’ in a cell, providing the site for much of the cell’s chemical activity and manufacture of protein-building blocks. So you can think of it as something like the factory floor to the nucleus’s administrative HQ.

During the creation of the cloned Dolly the sheep in 1998, through to the first cloned rhesus macaque monkey embryos in 2007, it was this nucleus-cytoplasm status quo that scientists considered to be essential. In order to clone the sheep and the monkeys, researchers destroyed the DNA-containing nucleus of an unfertilized egg and replaced it with the nucleus of an adult cell. An electric shock was used to activate the egg, instead of fertilization with sperm, and the resulting embryos – which were genetically identical to the adult cell but had no resemblance to the egg donor – were implanted into the womb of a surrogate mother.

Paradoxically, research conducted in the 1960s had indicated that if you take the nucleus from one egg cell and place it into another, the nucleus that was introduced would adopt the behaviour of the host cell rather than the host cell taking instructions from its new nucleus. The cytoplasm was dictating orders to the chromosomes in the nucleus, ‘telling’ the egg whether or not to divide and mature – a case of the body controlling the brain, as it were, instead of the other way around.

In 1971, Yoshio Masui and Clement Markert of Yale University set up an experiment to work out what exactly in the cytoplasmic soup was pulling the nucleus’s strings. They found two powerful ingredients. The first they called maturation promoting factor, or MPF, because it puts a cell on the road to mitosis or meiosis. The second they called cytostatic factor, or CSF. It is CSF that prevents an egg from developing into an embryo. CSF stalls meiosis in the egg through a delicate communication system of proteins. One of the proteins certainly involved is Mos, which is made before the early egg embarks upon its first meiosis. If Mos is injected into a normally dividing embryo, all cell division stops. After successful fertilization, Mos is destroyed in the cytoplasm, which allows cell division to get going. But Mos does not work on its own. Another protein, called Emi2, also helps to stop an egg from becoming an embryo. All of this intricate chemical activity seems to exist for just one reason: to stop virgin births from occurring. Indeed, c-mos, the gene that encodes the Mos protein, is a growth-controlling gene that has the ability, if it is mutated or otherwise unregulated, to cause a tumour to form.

This connection between unregulated tumour growth and very regulated egg growth was tantalizing to scientists. So, in 1994, a team of researchers based at the University of Cambridge and New Zealand’s Ruakura Agricultural Centre created mice with a shorter than normal version of the c-mos gene. The smaller Mos protein produced from this mutant gene did not work and was unable to order around the cell in its usual way. In many of the mice with the defective Mos, eggs spontaneously divided – parthenogenesis. And one in three of these mutant mice developed ovarian teratomas.

This seemed to be unmistakable evidence that the development of ovarian teratomas is related to mistakes in the c-mos gene. Except we know that the Mos protein does not play any significant role in the development of ovarian teratomas in humans. Human ovarian teratomas may come about because of mutations in any of several genes that, in their normal forms, make proteins that hold a cell’s development at bay, including Emi2.

What else could make an unfertilized egg start dividing? It has long been known that fertilization by sperm triggers a surge of calcium into the egg. Indeed, in the lab, adding calcium to an egg is routinely used to start parthenogenesis. This offers scientists another candidate protein: calcineurin. Calcineurin is involved in immune system function, putting T cells into action, and mutant mice that cannot produce it exhibit behaviours similar to symptoms of schizophrenia. Calcineurin should be dependent on the presence of calcium to work, but a genetic mutation might allow it to work on its own.

Finally, teratomas must get around the requirement for other, non-genetic components, such as the centriole, which are normally inherited from the father. In many species, including worms, snails, fish, and amphibians, the requirement for centrioles is the main preventative measure against virgin birth. In mammals, however, the process of moving the chromosomes around in the cell is a little more complicated. For instance, unfertilized mice eggs have centrioles, which organize the chromosomes inside. Human eggs also have centrioles, but they do not work, which is why human embryos inherit centrioles from the father. Maybe, once in a blue moon, those maternal centrioles have some say in what’s going on in the egg.

In the Palais des Beaux-Arts in Lille, France, hangs a desolate but fantastical painting, The Concert in the Egg based on a drawing by the Dutch master Hieronymous Bosch. In it, you are confronted with an impossibly large egg, flanked by two withered trees