The power of plasticity as a process of adaptation and evolution is very much a consequence of the way in which it provides phenotypic variation that, rather than being random, is directly related to the nature of environmental challenges. In doing so plasticity reduces the immediate effect of changes in environmental conditions (be they competition, habitat loss, food availability, predation, altitude, etc.), adjusting phenotypes to positions on their ranges that are adaptive. In the longer term, if the environmental condition is maintained, natural selection may act permanently to shift to this adaptive position. Plasticity, then, is a mechanism of adaptation and consequent evolution. An example of a mechanism of how plasticity works (as opposed to what it does) demonstrates another departure from the random mutation based concept of adaptation.
Crude oil pollution is dangerous to most organisms and their habitats partly because of its viscous nature (as in major accidental spills) and partly because of the large number of toxic chemicals it contains. Fish are among the organisms exposed to oil pollution and its poisonous effects, which often involve interference with embryonic development resulting in reduced hatching and hatchling survival, morphological deformation, biochemical and neurological alteration, and behavioural change. These effects are of interest to scientists because of their ecological importance and the insight they can provide to cellular and developmental processes. Zebrafish (Danio rerio) are frequently used for laboratory studies in this area of environmental science.
In the study in question1, adult zebrafish (Danio rerio) were exposed in their diet to an extract of crude oil containing many of the chemicals known to cause the oil’s toxicity. After a period of this treatment the fish were mated and progeny larvae also subjected to oil exposure. Both the parent adults and the larvae were subjected to a range of tests for any effects of the oil on their tissues and health. Oil treatment had no effects on the morphology or general health of the adult parental fish, though their fertility was reduced. Larval progeny are known to be particularly sensitive to chemical pollutant exposure, and this was confirmed by comparing the effect of oil on progeny from untreated parents; they had reduced survival compared with an untreated cohort.
However, larval progeny of oil treated adults were partially resistant to this oil toxicity; survival of populations of these larvae was 30% greater than oil treated larvae from parents that had not been exposed to oil. The extent of phenotype change in the progeny from oil treated parents became even more apparent with the observation that their survival decreased when they were raised in clean water with no oil exposure. These larvae are therefore phenotypically adjusted to the oil contaminated environment. The striking aspect of these results is that the phenotypes of the progeny larvae is dependent on the experience of their parents; even though parent fish have been minimally affected by oil, their treatment has promoted a change in their offspring. This is an unexpected observation because though something passed from the parents is causing the phenotype change (i.e. it has been inherited), that heredity cannot have occurred through a genetic mechanism (the rates at which genetic mutation and other genetic changes occur mean that it is impossible that the toxicity resistance arose in this way in such a high proportion of affected larva). Instead, this transgenerational transfer of toxicity resistance appears to be an ‘epigenetic’ effect, i.e. a heritable change in gene function that has occurred without a change in the DNA sequence.
”Larval progeny of oil treated adults were partially resistant to this oil toxicity”
”That heredity cannot have occurred through a genetic mechanism”
”Chemical marking of genes in these ways enable gene expression patterns, and hence phenotypic traits that are variable, to be transferred from one generation to another.”
Over a century of genetic science established and increasingly supported a heredity mechanism based entirely on the code contained in organisms’ DNA. That view has altered substantially in recent years not least because advances in research techniques have revealed how additional features of genetic material influence how genes behave. It is beyond question that DNA is the principal transgenerational carrier of hereditary information in the form of the genes that it encodes. Biota and cells are their phenotypes, and phenotypes are the combined result of the genes carried by organisms and the patterns in which they are expressed. It follows that if specific combinations of expressed genes can be maintained between generations then that provides another contributor to heredity, one that potentially introduces the influence of parental condition and experience to it.
That argument was long countered by the fact that during animal reproduction adult patterns of gene expression appear to be stopped. However, recent research into how other molecules initiate or repress gene function by physically and chemically interacting with DNA has revealed that there are notable exceptions to this resetting of gene expression. Two types of such interaction are of interest here. These are methylation, the addition or removal of small chemical groups to DNA nucleotides, (the four components whose sequences comprise its coded information), and the addition or removal of chemical groups to histone proteins, which are important components of the complex structures in which DNA is mounted and that are important in the mechanisms of gene function. The chemical marking of genes in these ways enable gene expression patterns, and hence phenotypic traits that are variable, to be transferred from one generation to another. (There is a further biomolecular entity that causes epigenetic effects which will be discussed later.)
See a summary diagram of epigenetic marking.
A recent study related to climate change that further illustrates inducible epigenetic marking and its inheritance is described in the next section.
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References
- Bautista, Naim M., and Warren W. Burggren. ‘Parental Stressor Exposure Simultaneously Conveys Both Adaptive and Maladaptive Larval Phenotypes through Epigenetic Inheritance in the Zebrafish (Danio Rerio)’. The Journal of Experimental Biology 222, no. Pt 17 (5 September 2019). https://doi.org/10.1242/jeb.208918 [↩]