Identical twins are not as identical as you might think. The differences may help to illuminate a process called epigenesis, which allows characteristics to be inherited in a way that is partly independent of the composition of their DNA. Identical twins are born from a single fertilised egg, or zygote. Genetically speaking, therefore, they are indeed the same. The effects of gestation are neatly set aside in such comparisons, since all co-twins share a uterus. However dizygotic twins share no more DNA than ordinary siblings. So if one monozygotic twin, for example, develops an ailment that the other escapes, the culprit is probably environmental. Conversely, when identical twins prove more likely to share a disease than dizygotic twins, the difference is chalked up to their genes. It is not, however, enough for organisms to share DNA in order to share characteristics. Those genes must also behave in the same way. One of the ways that the behaviour of genes is regulated is by the application to their DNA of particular clusters of atoms, known as methyl groups. Methylation shuts a gene down. To the extent that the pattern of methylation is passed from parent to offspring, it forms a second, “epigenetic”, inheritance mechanism parallel to the primary DNA-based one. A significant amount of variation between twins is found, possibly enough to explain why apparently heritable diseases that require the coincidence of several genetic risk-factors do not, in practice, always appear in both twins. Schizophrenia, for example, has a family component. But if one twin of a monozygotic pair develops it, there is only a 50% chance that the other will too, rather than the 100% chance that you would see if the sequence of genetic “letters” in the DNA were the only cause. Results suggest that although monozygotic twins do differ epigenetically, they differ less than dizygotic twins. This is actually very confusing. The prevailing wisdom about epigenesis is that most existing methylation is erased when the eggs and the sperm are maturing. That should stop epigenetic patterns being passed on, and allow new ones to be imposed to suit the needs of the newly created organism. Indeed, there are several waves of epigenetic reprogramming during an embryo’s development. That some methylation escapes pre-fertilisation erasure has been suggested by experiments on other animals, but this has been thought the exception, rather than the rule. If that were so, though, the degree of difference between identical and non-identical twins would be broadly the same. It is not. Quite a lot of pre-existing methylation is making its way into the new individual—and thus providing both a complication to those who try to understand the intricacies of inheritance, and a promising new line of inquiry.
We are a long way from being able to control any of this - if we were were might well be able to epigenetically engineer. This would include the ability to transfer lifetime learning other than by teaching. My first thoughts are that this is a bit like the dreaded Microsoft updates. Later ones concern the complexity of information systems in the production of what we are - what might lie beyond the smallest we can now reach - a world of information. --~--~---------~--~----~------------~-------~--~----~ You received this message because you are subscribed to the Google Groups ""Minds Eye"" group. To post to this group, send email to [email protected] To unsubscribe from this group, send email to [email protected] For more options, visit this group at http://groups.google.com/group/Minds-Eye?hl=en -~----------~----~----~----~------~----~------~--~---
