Evolving ideas

(John Jacob Lyons, 18 September 2009)

The four dimensions of evolution identified in Jablonka and Lamb’s book ‘Evolution in Four Dimensions’ were described as; genetic, epigenetic, behavioural and symbolic. Although this is an extremely useful book, the dimensions proposed are not considered the best basis on which to carry forward research on evolutionary theory. The ‘symbolic’ dimension relates to one particular aspect of cultural evolution and, although there can be interaction between adaptive cultural change and genomic change, the use of the word ‘symbolic’ appears inappropriate and too narrow to denote this interaction. Genetic and epigenetic processes often operate in tandem and it may be misleading to nominate them as separate dimensions. An important deficiency is that the nominated dimensions are not from the same class of objects. They are not separate and different evolutionary processes and neither are they separate, independently generated drivers of evolution.

I want to suggest three independently generated, primary drivers of evolution at organism level that, I believe, would provide a better basis for future research; random genetic mutation, natural environmental change and behavioural change – including niche construction.

These categories can all be described as independent drivers of evolution. They are mutually exclusive but, of course, not exhaustive at this level of analysis. Sexual selection is a powerful driver and species would still evolve within the constraints of their existing gene-pool and without considering new mutations. Then there are the effects caused by artificial human selection; both within the human species (eg contraception) and those imposed on other species (eg selective breeding). However, I have highlighted three evolutionary drivers that, I believe, have been somewhat confused in previous work in evolutionary theory.

Each of these primary drivers is described below in a little more detail below.

Driver 1 – Random genetic mutation

This is often called (Classical) Darwinian Evolution. A mutation of this kind will be adaptive if it results in an adaptive phenotype; either increasing the viability/ fecundity of the organism or increasing both. The expected incidence of the mutation in the next generation will increase and will increase further in future generations as long as the mutation continues to be adaptive.

Driver 2 – Natural environment change

Particular extant alleles of particular genes/ epigenetic-markers will be more adaptive in the changed environment, again resulting in an expected increase in the incidence of this particular allele-set in future generations.

Driver 3 – Behavioural change – including niche construction

Initially, one or a small number of organisms learn a behaviour that proves to be adaptive. This behaviour may or may not affect the physical environment. Manifestation of the adaptive behaviour will often be positively and causally correlated with particular allele-sets that make the organism more likely to manifest the behaviour.  Selection pressure will result in an increase in the expected incidence of the allele-sets’ constituents in the following generation (see Behavioural Genetic Priming). This will, in turn, increase the expected number of organisms manifesting the behaviour in that generation. This positive feedback loop will continue to increase the incidence of the adaptive behaviour in future generations. In due course, all organisms in a population may be, to a greater or lesser extent, genetically primed to manifest the behaviour with a minimal trigger from the environment. I say “to a greater or lesser extent” since there may well be other adaptive behaviours and other sources of selection pressure in play that are underpinned by overlapping gene-sets. This would eventually result in optimal allele configurations for the complete set of adaptive behaviours and other sources of selection pressure but a suboptimal configuration for any particular adaptive behaviour.

Driver 3 can be described as an adaptive acquired characteristic and, although the characteristic itself cannot be assimilated into the genome, its positive association with concomitant, genetically mediated predispositions means that it is ‘able’ to prime the genome to increase manifestation.

If we add back the other drivers of evolution previously mentioned we get:

Driver 4 – Sexual Selection

Driver 5 – Natural Selection within current gene-pool

Driver 6 – Artificial Human Selection

Driver 7 – Hybridisation

Is this an exhaustive set of evolutionary drivers?

(prepared 14 June 2009 by John Jacob Lyons)

The ‘Baldwin Effect’ has been defined as an adaptive trait change in an organism – that occurs as a result of its interaction with its environment- becoming gradually assimilated into its developmental genetic/ epigenetic repertoire. My ‘genetic priming’ hypothesis seeks to clarify the process involved in the Baldwin Effect and to correct several points in the definition above that relate to the effect of this process.

The process consists of an inter-generational positive feedback loop between the adaptive trait and the positively and causally correlated subset of the genome that tends to support the trait. This is described in greater detail in my article in the ‘Evolving Ideas’ blog. As stated there, selective pressure will result in the manifestation of the trait earlier and earlier in the development of the organism.

However, the adaptive trait will never be “ – assimilated into its developmental genetic/ epigenetic repertoire.” What will happen is that selective pressure will result in the allele-configuration of the relevant subset of genes ‘trying’ to change in order to optimize the support given to the trait. In doing so, it may well be in competition with other adaptive traits ‘trying’ to optimize the subset to support them. This will obviously result in sub-optimization for any particular individual trait. The ultimate result will be that the genome will have been, within the aforementioned constraint, primed to support the manifestation of the original adaptive trait. An example will make some of these points clear.

It is well known that, over the human EEA, post-weaning lactose tolerance developed in temperate regions in which cattle were farmed. In this case, the adaptive trait was milk consumption (Vitamin D enables absorption of calcium; particularly adaptive in temperate regions) and the correlated subset of the genome was that involved in controlling lactose tolerance. The positive feedback explained above has resulted, in these regions, in the ubiquitous priming of the human genome toward post-weaning lactose tolerance and not in a genetically assimilated tendency to consume milk! There has been no assimilation of the adaptive behaviour; only genetic priming of the associated subset of the genome.

I suggest that, subject also to many relevant cultural evolutionary factors of course, humans have been genetically primed for language, religiosity, morality and love/ attachment/ empathy in a similar way.