Genetic theory has been galloping along nicely to the stage where we know that we inherit two copies of each gene, one from Mum and one from Dad. The general idea is that both copies are active within the cells of the offspring. However, some deviant genes see fit to break this rule and, while inheriting a copy from both of our parents, only one copy is switched on. For certain genes, it is only ever the mother's version that is active, whilst for other genes it is the copy inherited from the father. Such genes are known as imprinted genes, and have been shown to be very important in mammalian development and disease (see figure below).
In the past few years, new data has come to light suggesting that imprinted genes may also have important effects on our behaviour. For example, in 1998 Professor Azim Surani's team in Cambridge discovered an imprinted gene, called Mest, controlling some aspects of "mothering" behaviour in mice such as nest-building. It is also required for growth of the developing baby. In the case of Mest only the copy of the gene inherited from the father is expressed, hence Mest is known as a paternally expressed gene. It was the first imprinted gene to be definitively shown to affect behaviour in mammals, and it is highly likely that there is a human version as well.
All very interesting, say the journalists, as they start painting gloomy pictures of scientists meddling with our genes, or mothers pleading genetic incompetence when they abandon their children. But the real significance of the Mest discovery is not what it can tell us about human behaviour, but what it can tell us about the battle of the sexes on a molecular level. When it comes to reproduction, male mammals, such as mice, have it easy. In order to spread their genes as widely as possible, they are under little evolutionary obligation to stay and nurture their progeny. But in a highly promiscuous species such as the mouse, where even littermates may have different fathers, imprinted genes such as Mest provide an insurance policy for the paternal genes by ensuring that foetuses will grow vigorously, and thereby use as many resources from the mother as possible.
Consider the evolutionary logic behind this: if there is no guarantee that the female's other offspring are the progeny of a given father, then it is in that father's interests to sap as much of the mother's strength as possible, and in the mother's interests to stop this happening for the sake of her genes (in the form of her future babies by other fathers). If a growth gene like Mest is only ever expressed from the father's copy, then this helps to ensure big, bouncy, baby mice. All very well from the father's point of view. But what can the knackered females do to retaliate? Use their own genetic armoury, in the form of other imprinted genes. For example, let me introduce two more genes: the insulin-like growth factor 2 (IGF2 for short) and its receptor, known as IGF2R. IGF2 stimulates growth of the embryo and is paternally imprinted (expressed from the father's copy). Conversely, the receptor is expressed only from the maternally inherited gene. It is thought that the mother's receptors help to "mop up" excessive paternally expressed growth factor, and so prevent the foetus from growing too large. In this way, we see a balance emerging between the paternally expressed genes striving to grow the biggest baby possible, and the maternally expressed genes, attempting to keep the situation under control. This balance is described as the "conflict theory of imprinting"- the true battle of the sexes on a microscopic scale.
So what can these studies tell us about ourselves? Firstly, rather than focusing on the big, flashy headlines of science stories we should be looking deeper into the significance of new findings, and secondly that the battle of the sexes goes much further than men always leaving the toilet seat up...