As I discussed yesterday, a recent publication by Eric Bapteste and his colleagues describes how external genetic change may be caused by a species living within another species (endosymbiosis). One of the paper’s key points is that species do not exist in isolation. They are surrounded by other species (often sharing the same body), and therefore may interfere with one another’s fitness.
Bapteste et al. explain how a species, for its own benefit, may cause “age-distortion” in another species using selfish genetic elements. (Teulière, Bernard, and Bapteste 2021) Age-distortion happens when a species living within another species carries and integrates genetic information that interferes with the aging of its host. Age-distorters are typically viruses, parasites, and symbionts. The host organism may end up aging if the age-distorter forces reproduction at an age-related cost. In other words, the fitness of an organism may be affected by the organisms living inside it. Age-distortion is a bit like the engineering concept of trade-off. It demonstrates that while external genetic change can bring about novelty, that novelty also has a fitness cost associated with it. The fitness cost might come from gene expression or just from copying the DNA.
Age-distorters cause mutational accumulation in their host, an external source of genetic change. The key point here is that mutations are not always due to the internal processes of an organism. This must be accounted for correctly when doing phylogenetics. Mutational accumulation in organisms cannot solely be attributed to internal polymerase errors or environmentally induced mutations. Fitness loss or enhancement must be considered within the broader scope of the ecosystem.
Why External Genetic Change Cannot Explain the Arrival of Genetic Information
External genetic change from age-distorters can contribute genetic novelty to a species. But what about original genetic novelty? When a microbiologist transfers DNA into E. coli using Phage P1 (called transduction) and the bacteria are plated on Kanamycin (an antibiotic), surviving colonies are an example of an externally sourced genetic change. The molecular reason that the colonies survived is they were given DNA by Phage P1, and that DNA contained a Kanamycin antibiotic resistance cassette. Thus the genetic change was external to the organism, E.coli.
Now imagine that the antibiotic resistance cassette, although helpful if trying to survive on Kanamycin, is also expensive for the bacteria to make and therefore drains the organism. In that case, over a lifetime it will reduce fitness in other areas and shorten lifespan. If this is the situation, the Kanamycin cassette would be considered a trade-off. This would also be an example of age-distortion.
Now the big question: Can this type of genetic change account for new genetic information? It could account for the arrival of novelty in the organism to which genetic information was introduced. But it cannot account for the initial arrival of new genetic information. See here from the chapter on “Sources of Variation” in the textbook An Introduction to Genetic Analysis (7th Edition):
For a given population, there are three sources of variation: mutation, recombination, and immigration of genes. However, recombination by itself does not produce variation unless alleles are segregating already at different loci; otherwise there is nothing to recombine. Similarly, immigration cannot provide variation if the entire species is homozygous for the same allele. Ultimately, the source of all variation must be mutation.Griffiths et al. 2000
By mutation, the authors mean environmentally caused or random polymerase mistakes. But wait… Aren’t somatic hypermutation, inter-family genetic change, and intra-family genetic change sometimes given as explanations for the arrival of genetic information? Is this ascribing more power to natural selection and random mutation than that combination really possesses?
As I stated already, genetic change has many sources. Clarifying the sources can help us understand what questions to ask when we observe genetic change over time in species. However, mechanisms of genetic change that could account for the arrival of the code of life can only come from a few categories: internal random copy errors, or external sources of genetic change from the environment, or from intelligence. This is because, apart from internal random copy errors, internally sourced genetic change is derived from the code itself. Programmed reassortments are design features of DNA that cannot explain the arrival of the code. Borrowed code from external species can also confer fitness advantages and disadvantages to the recipient organism but it cannot explain the origin of the code to begin with. Externally sourced genetic change that could account for the arrival of the code of life must come from chemically induced mutagenesis, UV radiation, or an intelligent agent.
Why Intelligent Design Is a Helpful Hypothesis
Thinking outside the box is always good. Intelligent design is the scientific hypothesis that the best explanation for the origin of certain features of the universe and living things is an intelligent cause. Regardless of whether one agrees with this hypothesis, it is certainly outside the box from mainstream evolutionary theory, which implies that material mechanisms alone can account for the arrival of all genetic information in living organisms. Interestingly, with advances in modern molecular and systems biology, mainstream evolutionary theory has faced increased criticism. As a competing hypothesis, intelligent design can help scientists recognize oversights, think differently about data, pose new questions, and recognize key challenges that would be missed without a competing model. Importantly, intelligent design does not exclude other material sources of genetic change as contributors to genetic change. It merely says that one additional plausible source for such change in organisms is an intelligent agent. The idea that an intelligent agent can be the origin of genetic code is highly consistent with our own observations that humans (as intelligent agents) create codes and languages and, in recent years, genetic change.
So how should researchers think about genetic change? What organizational framework should they use? Can we assign a source to all genetic change? Let’s think deeply about these questions.
- Di Noia, Javier M., and Michael S. Neuberger. 2007. “Molecular Mechanisms of Antibody Somatic Hypermutation.” Annual Review of Biochemistry76: 1–22.
- Griffiths, Anthony J. F., Jeffrey H. Miller, David T. Suzuki, Richard C. Lewontin, and William M. Gelbart. 2000. Introduction to Genetic Analysis. W. H. Freeman.
- Teulière, Jérôme, Charles Bernard, and Eric Bapteste. 2021. “Interspecific Interactions That Affect Ageing: Age-Distorters Manipulate Host Ageing to Their Own Evolutionary Benefits.” Ageing Research Reviews 70 (May): 101375.