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On the 4th. August, 2003, the New Scientist published a report entitled "You are what your mother ate, suggests study"(1) The study was one about epigenetic gene regulation, which the New Scientist referred to as "a weird form of inheritance." This leads us to wonder what we mean by inheritance in a genetic, and, in most people's minds, Darwinian, context.

The word epigenesis originated in the eighteenth century in the debates about preformation. The preformatist view held that "all major structures of the adult are already preformed in the sex cell . . . ."(2) Epigenesis held that "morphological complexity develops gradually during embryology from simple beginnings in an essentially formless egg". At that time "that complexity must be imposed from without by some vital force . . . ."

Once DNA was discovered, the meanings changed slightly, for the organism could be said to be preformed by the set of instructions held within the genetic code, while, in a more secular age, epigenesis was held to be the effect of the environment in shaping the way those instructions were read. But this would seem to be more to do with ontogeny, the life history of the individual from conception, than phylogeny, the history of the species.

We, of course, inherit much more than our genes. We inherit our family's wealth and its social position. If we live in a family of gluttons, regardless of any genetic predisposition, we may become obese. The environment we grow up in, and in the womb, may affect our development, even the way our genes are expressed, in ways that are still not fully understood. But to suggest that such environmental influences are passed on to future generations carries an air of Lamarckism.* We will, therefore, use this study(3) as an example to tease out the word's actual meaning.

The study concerned mice of a particular colour called 'agouti' which occurs because of a yellowing of otherwise black hair, due to the production of phaeomelanin instead of eumelanin, producing the brown colour of wild-type mice. The loss of this effect in black mice is caused by a mutation, a so-called transposable element in a particular gene. Such transposable elements, colloquially known as 'jumping genes', are quite common in mammals and, for instance, constitute over thirty-five per cent of the human genome. The majority are normally silenced by a process called methylation. A particular diet for a mother can affect this methylation in her offspring, and hence their coat colour.


 Well and good, but this seems no different from, for instance, a child inheriting its mother's heroin addiction.

The germ cells in mammalian mothers are formed very soon after conception and then remain dormant until puberty. Accordingly, the researchers took dams that were known to be virgin, and fed them a vitamin-rich diet for two weeks before they were mated. The effect on coat colour and presence of methylation was observable in the young, and persisted until adulthood.

Moreover, even though they ate a normal diet, the effect was still, to some extent, observable in their offspring, the 'grand offspring' as it were, of the original mothers, but would be expected to disappear in future generations.

The point of this particular study was to show that dietary interventions in humans may have unintended consequences, not simply metabolic, but genetic, on, for instance, the susceptibility to disease.

For our point of view it illustrates that the genome is less rigid than Darwinian theory would predict. The latter gives a view of the genome unchanging across many generations, perhaps thousands of years - such change depending on random mutational events. Here we have an example of the flexibility (and self-regulation) of the genome as it responds to the environment within generations.

Some instances last for hundreds of generations however, without obviously coming about because of the external environment, and the word epigenesis has come to mean more literally "over" or "around" the gene. In other words, influences on genetic function that are transmitted through mitosis and meiotis, but without changing the DNA sequence. Examples of this are the inactivation of one X chromosome by methylation in females, and a newly discovered phenomenon by which one of a pair of otherwise identical genes may be imprinted such that it is activated or inhibited by one of the parents.

Some authors look to epigenesis as a mechanism which enables adaptation and speciation to occur more quickly than by the orthodox Darwinian route.

* In the eighteenth century, many people were attempting to explain evolution. Lamarck proposed that it was due to "Inheritance of acquired characteristics."

Bibliography and good reading.

  1. New Scientist 04 August 03 "You are what your mother ate, suggests study"
  2. Gould, S.J., (1977) Ontogeny and Phylogeny, Cambridge: Belknap Press
  3. Waterland, R.A., Jirtle, R.L., (2003) Transposable Elements: Targets for Early Nutritional Effects on Epigenetic Gene Regulation, Molecular and Cellular Biology, 23 (15) August pp5293-5300

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Bland, J., (2003) About Gender: Epigenesis
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