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

develop; when they did the same with DNA only from eggs, the embryos developed normally but the placenta and other supporting tissues failed to thrive.

But this raises a more perplexing question. Why would a father’s genetic contribution be necessary in making a placenta, when viral DNA appears in the genome of both sexes? Why didn’t evolution give females the capacity to make a placenta all on their own?

The evolution of the placenta must have been something of a double-edged sword for our ancestors. While being able to gestate inside an adult afforded unprecedented protection for vulnerable young, mammalian embryos functioned like a parasite on the mother. Apart from the challenges to the mother’s immune system, the embryo drained nutrients via the newly designed placenta. This nutrient flow has to be regulated by the body, so that neither mother nor embryo is starved. Ancient viral DNA cannot handle this; new genes with new instructions had to tackle the task.

Not all genes in our cells work all of the time or in all parts of our bodies. Some, for instance, only work in the limbs when a foetus is developing in the womb; some only in the brain of an adult. As this indicates, genes have to be turned ‘on’ to have an effect, a phenomenon known as gene expression. Gene expression can be understood as the process by which the letters of the DNA code are ‘read’ and start the production of certain proteins, which tell cells (and thus everything in the organism) what to do and when to do it. For some parts of the genome in animals, the expression of a particular gene is determined by whether it was inherited from the mother or the father.

As the placenta gradually evolved in mammals, evolution had to find a way to tell the viral genes and the newer genes when to start working and when to stop. Sometime around a hundred and forty-eight million years ago, certain genes vital for the healthy development of the placenta started to become locked and unusable – coded so that they could never be read, or expressed, since they sometimes mucked up the works. So even though the mother’s genome still contains all the genes it takes to grow a complete baby from one of her eggs, only some of them are allowed to function. The same is true for some of the father’s genes. This sexual selection in whether a certain gene can be expressed is called genomic imprinting.

There is nothing inherently ‘wrong’ in the coding of these genes that don’t work. Imprinting doesn’t involve a mutation or a mistake that stops the gene from working – think of it as a padlock that means the gene’s DNA cannot be accessed. But just as a door can be opened if you find the right key, imprinted genes can be unlocked, even erased, by different conditions. The process is by no means static. And of the twenty-three thousand human genes that can be expressed by making proteins, only about eighty are ever silenced by imprinting. What is interesting is that many of these genes that are imprinted dictate not what we will look like, but are able to manipulate the growth and nutrition of the foetus in the womb. It seems that when evolution invented sex, it used imprinting as a way of ensuring that the female needed the male to reproduce. The health and survival of any offspring depends heavily on the father’s genes for making the placenta, since the mother’s genes have been locked. It seems that sperm do more than just deliver packets of DNA into eggs – they regulate pregnancy itself.

Imprinted genes, like viral DNA, are a frontline in a battle: two beings fighting over scarce resources, with some genes trying to ensure the best result for the child at the expense of the mother, and others, for the mother at the expense of the child. The majority of genes that are locked in the mother’s DNA but not in the father’s directly influence how many nutrients a foetus is able to extract from the mother’s body. A father’s genes benefit if his offspring are larger and stronger when they are born, because that gives them a better chance of surviving to adulthood and the father’s genes being passed on further – for the father, there’s no personal risk involved. In contrast, many of the mother’s genes that do work at this stage are trying to curb the foetus’s growth – to keep those nutrients for the mother. Consider, too, that if every time she became pregnant, the mother could restrict foetal growth, she would secure a better chance of producing more children from limited resources, and she would be less likely to die from complications of childbirth. Evolutionarily speaking, this is to the advantage of her genes, which would have more opportunities to be passed on to a future generation.

This strategy is custom-made for polygamous reproduction. When each female regularly bears offspring of several different males, the mother has an equal genetic stake in each embryo and will achieve the best outcome for her genes if resources are allocated equally to each one; the father is better served, however, if his particular embryos grow faster and extract a greater share of resources from the mother than do the siblings in which he has no genetic stake. So silencing certain genes in the placenta ensures that every foetus has an equal chance of survival. The ability of a father’s genes to influence how an embryo acquires resources from its mother is rare, but it does also appear in some plants. In these plants, including maize (Zea mays, or corn), the mother nourishes the growing embryo for an extensive period after fertilization, whereas the father experiences negligible costs – just its seed.

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