Seeds develop similarly within the bodies of their parents, but they are fed via an endosperm rather than a placenta. Normal imprinting in both placenta and endosperm are critical to healthy embryonic development. In both species these organs provide the interface for maternal-foetal dialogue and are thus key players in regulating embryonic growth. Wolf Reik (Babraham Institute, Cambridge, UK) has studied Igf2 behaviour in mice. He notes that imprinting of Igf2 is critical for normal placental growth. Knock-out the gene in the placenta and foetal growth is restricted.
 
Some scientists believe that imprinting evolved in species with a placental-habit to cope with greedy infants that might take more than their fair share of the resources. This school of thought is based on the ‘parental conflict theory’ proposed by David Haig (Harvard, USA). Mum needs to make sure she saves some strength for herself and your siblings, so her genes have evolved to temper foetal growth. So why do father’s genes want you to be bigger? Well, in general babies that are slightly bigger than average have better survival prospects. Of course, it is not really a case of your genes having their own will, but merely that any genes that promote survival tend to get passed on.

Beyond the special case of imprinting, silencing by means of DNA methylation represents the evolution of a primitive immune system. Around half of our genome is silent, made up of nonsensical repeats that don’t contain the instructions to make protein. Some of them can hop around in the genome, a behaviour that can have fairly disastrous consequences for the function of neighbouring genes. How did they get there? There are no definitive answers but some look and behave like viruses, well-known stowaways in the genome. Cells seem to mark repeat sequences with methyl to shut them up, which serves to protect our genes. As Denise Barlow (University of Vienna, Austria) has suggested imprinted genes may have arisen accidentally, the result of DNA methylation spreading to other regions of the genome. She points out that this accident must have had some evolutionary advantage to have caught on, although the matter is still open for debate.

Throughout our lifetime and across evolutionary time, silencing DNA has allowed both our cells and us to evolve different habits. Consider for a moment the riotous din of 30 000 human genes were a large proportion not switched off. We don’t need to use all 2m of our DNA within every cell. Furthermore, you wouldn’t want the cells in your eyeballs to make fingernails. Ligers and tigons show us that the same DNA can have very different consequences depending on how it gets packaged up by their parents. DNA sequences don’t paint the whole picture. Their revelation is only the beginning. The blueprint alone holds the potential for life, but life is everything that happens beyond DNA.