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

its chromosomes, you start to see the growth of abnormalities and, later, tumours. An inability to repair DNA seems to be an important part of why women’s ovaries age, and that’s where BRCA1 comes in. Manipulating the genes that are involved in DNA repair could be one way to avert failing ovaries in the future. Further, new bits of genes on chromosomes 13, 19, and 20 have been found that influence the age at which a woman experiences menopause, as well as ageing-related diseases such as breast cancer, osteoporosis, and cardiovascular disease.

For a woman facing the dilemma of focusing on career or childbirth in her twenties or thirties, being able to predict the age at which she might begin to have serious difficulty in becoming pregnant would be the holy grail of family planning. The decision isn’t binary, however: it’s not a choice between pregnancy now or never. A woman who wanted to focus on her professional ambitions for the next decade already has the option of freezing her ‘young’ eggs for use in the future. But at a cost of £3000 per attempt, and some women having to undergo three rounds of extraction to get a good harvest of eggs, most women, without sure information, will be likely to defer until later. In the future, gene therapy may also be developed to reinstate the functioning of what is normally lost after menopause, affecting the treatment of fertility and age-related diseases. Such therapies might even extend the life span of a woman’s ovaries and allow a woman to remain ‘naturally’ fertile for far longer than has ever been possible. An ‘old’ mother in the future will probably bear little resemblance to the ‘old’ mothers who hit the front pages today: she would not have needed IVF or a donor egg, because she will be able to use her own, without detrimental effect on her health or life expectancy. Scientists are still uncovering exactly which genes will be useful or amenable to manipulation, but the research is already in full swing.

If the human X chromosome sometimes harbours genes that can cause problems for female fertility, the Y chromosome can be viewed as a disaster zone. The Y chromosome, which once contained as many genes as the X chromosome, has deteriorated so much over time that it now contains fewer than eighty functional genes compared to its partner, which is large and packed with more than one thousand. This deterioration, according to geneticists and evolutionary biologists, is due to accumulated mutations, deletions, and anomalies that get stuck, in a way: they have nowhere to go, because the Y chromosome doesn’t swap genes with the X chromosome like every other chromosomal pair in our cells do.

With such a small number of genes to carry, the Y chromosome is small. It’s also peculiar, filled with many repetitive DNA sequences but not many genes. Unlike the X chromosome, whose genes display a variety of general and specialized functions, the Y carries the codes for only forty-five unique proteins. These proteins are the blueprints essential for the male reproductive system, particularly those important in sperm development. Of course, when an egg is fertilized, the sex chromosomes are matched up. In a woman, the two XXs pair up easily. But because the Y and the X are so different, in size and information, the match isn’t quite right. So in a man, the X and the Y align only in a small region, where you could say the chromosomes are singing from the same hymn sheet. This has helped to perpetuate the diminution of the Y – the parts of the chromosome that don’t match up with the X aren’t necessary; they’re expendable. Thus, the Y has slowly but surely become smaller and less genetically rich compared with its sex partner.

Technically, it’s not simply having a Y chromosome that makes a person male, it’s having the right bits of the Y – the right key genes, known as testes-determining factors. The most important gene of this group is SRY, for sex-determining region of Y, but there are almost certainly other genes that scientists have yet to identify. One case dramatically illustrates the role of SRY: the rare sex chromosome disorder known as de la Chapelle syndrome, also called XX male syndrome. Individuals with the syndrome appear to be male, though they have two X chromosomes and no Y – just like a woman. The critical difference is that the SRY portion of a Y chromosome has usually become attached to one of the X chromosomes. That small error effectively converts an X chromosome into a Y, female into male. The genetic mutation is sometimes evident in a short stature, an abnormally shaped penis, and the appearance of breasts. Curiously, there are a considerable number of cases in which XX males do not carry the SRY gene. Instead, these men have a closely related gene, called SOX9, which also causes skeletal deformations. As a result of these genetic anomalies, somewhere between one in nine thousand and one in twenty thousand men have XX chromosomes, rather than XY. Maleness – to some extent, depending on how you define it – is perfectly possible without a Y chromosome, or even the SRY gene.

Of course, one way in which we define maleness, socially, involves sexual reproduction. People with XX male syndrome have little or no detectable sperm in their semen, making them effectively sterile. Not having a Y chromosome is bad news for fertility. Take XX male cocker spaniels, for example – without the SRY gene, many turn out to be infertile hermaphrodites. There have also been several reported cases of XX male farm animals, including among pigs and goats. This is unfortunate news for the breeders who own a particular animal, but is not yet a threat to their