The Epigenetics Revolution

The raw material for random variation is mutation of the DNA sequence of the individual; his or her genome. Mutation rates are generally very low, and so it takes a long time for advantageous mutations to develop and to spread through a population. This is especially the case if each mutation only gives an individual a slight advantage over its competitors in a particular environment.

This is where the Lamarckian model of acquired characteristics really falls over, relative to Darwinian models. An acquired change in phenotype would somehow have to ‘feed-back’ onto the DNA script and change it really dramatically, so that the acquired characteristic could be transmitted in the space of just one generation, from parent to child. But there’s very little evidence that this happens, except occasionally in response to chemicals or irradiation which damage DNA (mutagens), causing a change in the actual base-pair sequence. Even these mutagens only affect the genome at a relatively small percentage of base-pairs and in a random pattern, so these still can’t drive inheritance of acquired characteristics in any meaningful way.

The overwhelming body of data argues against Lamarckian inheritance, so there’s very little reason for individual scientists to work on this experimentally. This isn’t surprising. After all, if you are a scientist interested in the Solar System, you could choose to investigate the hypothesis that at least some parts of the Moon are made of cheese. But to do so would mean that you wilfully ignored the large body of evidence already present against this – hardly a rational approach.

There’s also possibly a cultural reason that scientists have shied away from experimental investigations of the inheritance of acquired characteristics. One of the most notorious cases of scientific fraud is that of Paul Kammerer, who worked in Austria in the first half of the 20th century. He claimed that he had demonstrated the inheritance of acquired characteristics in a species called the midwife toad.

Kammerer reported that when he changed the conditions in which the toads bred, they developed ‘useful’ adaptations. These adaptations were structures on their forelimbs called nuptial pads, which were black in colour. Unfortunately, very few of the specimens were retained or stored well, and when a rival scientist examined a specimen he found that India ink had been injected into the pad. Kammerer denied all knowledge of the contamination and killed himself shortly afterwards. This scandal tainted an already controversial field[39].

One of the statements in our potted history of evolutionary theory was the following, ‘An acquired change in phenotype would somehow have to ‘feed-back’ onto the DNA script and change it really dramatically so that the acquired characteristic could be transmitted in the space of just one generation, from parent to child.’

It’s certainly hard to imagine how an environmental influence on the cells of an individual could act at a specific gene to change the base-pair sequence. But it’s all too obvious that epigenetic modifications – be these DNA methylation or alterations to the histone proteins – do indeed occur at specific genes in response to the environmental influences on a cell. The response to hormonal signalling that was mentioned in an earlier chapter was an example of this. Typically, a hormone like oestrogen will bind to a receptor on a cell from, for example, the breast. The oestrogen and the receptor stay together and move into the nucleus of the cell. They bind to specific motifs in DNA – A, C, G and T bases in a particular sequence – which are found at the promoters of certain genes. This helps to switch on the genes. When it binds to these motifs, the oestrogen receptor also attracts various epigenetic enzymes. These alter the histone modifications, removing marks that repress gene expression and putting on marks that tend to switch genes on. In this way, the environment, acting via hormones, can change the epigenetic pattern at specific genes.

These epigenetic modifications don’t change the sequence of a gene, but they do alter how the gene is expressed. This is, after all, the whole basis of developmental programming for later disease. We know that epigenetic modifications can be transmitted from a parent cell to a daughter cell, as this is why there are no teeth in your eyeballs. If a similar mechanism transmitted an environmentally-induced epigenetic modification from an individual to their offspring, we would have a mechanism for a sort of Lamarckian inheritance. An epigenetic (as opposed to genetic) change would be passed down from parent to child.

Heresy and the Dutch Hunger Winter