One of the more persistent creationist falsehoods is the claim that mutations can only damage or destroy genetic information and can therefore provide none of the variation needed for evolution. The claim is usually protected from contrary evidence by leaving “information” conveniently undefined or by dismissing every beneficial mutation as merely a “loss of function”.
However, a new study by Jasper B. Gomez, Jeffrey E. Barrick and Christopher M. Waters of Michigan State University provides an especially clear demonstration of mutation generating heritable variation on which natural selection can act. Their findings were published in Nature Microbiology.
The researchers found that the genomes of the bacteriophages T2 and T4 — viruses that infect bacteria such as Escherichia coli — contain regions of repetitive DNA called contingency loci. These are mutational hotspots in which the DNA-copying machinery is particularly liable to slip while copying a run of repeated bases. It may insert or omit one of the repeats, changing the way the remainder of a gene is read and consequently altering the protein it produces.
Such replication errors occur in these regions thousands of times more frequently than mutations across the rest of the phage genome. Far from producing a population of genetically identical copies, therefore, phage replication continually generates a mixture of variants with different inherited characteristics.
The discovery arose from experiments involving a bacterial antiviral system called TgvAB, normally found in Vibrio cholerae, the bacterium that causes cholera. The researchers transferred the genes for this defence system into laboratory E. coli and exposed the bacteria to T2 phages. Although the defence initially restricted the phages, the viral population began overcoming it within hours.
Genome sequencing revealed that many of the successful phages had acquired frameshift mutations within a repetitive region of a gene called agt. This gene encodes an enzyme that attaches glucose to modified cytosine bases in the phage DNA. That modification protects the viral genome against some bacterial restriction systems, including McrA and McrBC, but it also enables TgvAB to recognise and attack it. Mutations that disable agt can therefore protect a phage against TgvAB while simultaneously making it more vulnerable to other bacterial defences.
Consequently, there is no single version of the gene that is invariably “best”. A functional agt gene is advantageous when one type of bacterial defence is present; a frameshifted version is advantageous against another. Because mutations at the contingency locus arise rapidly and can be reversed by subsequent replication slippage, the phage population continually contains variants suited to different bacterial hosts. This is a form of evolutionary bet-hedging: not foresight or conscious preparation, but the production of heritable diversity followed by differential survival and reproduction.
The researchers also found numerous candidate contingency loci in T4 and across the genomes of diverse E. coli-infecting phages, suggesting that this capacity for rapid diversification is not confined to a single gene or phage strain. Natural selection has, in effect, favoured DNA arrangements that are especially capable of generating further variation in circumstances where the selective environment changes continually.
Of course, a frameshift may disrupt a protein, and many mutations will still be neutral or harmful. But that does nothing to rescue the creationist claim. Evolution does not require every mutation to be beneficial or to increase the length of a genome. It requires mutations to produce heritable differences, some of which confer an advantage in a particular environment. That is precisely what the researchers observed. A one-base insertion or deletion changed an inherited phenotype, altered which bacterial defences the phage could evade and affected which variants reproduced successfully. “Genetic information” is not a mystical quantity that mutations can only diminish; its biological value depends on what a sequence enables an organism or virus to do in its current environment.
The study also exposes another problem for claims of benevolent intelligent design. Bacteria possess elaborate systems for detecting and destroying invading viral DNA, while bacteriophages possess equally elaborate countermeasures for evading those defences, killing the bacteria and producing more viruses. An intelligent designer would appear to be arming both sides of a perpetual microscopic war. Evolution, by contrast, predicts exactly such an escalating arms race, with every successful defence creating selection for a counterdefence and every counterdefence creating selection for something capable of defeating it.
This evolutionary capacity may eventually be turned to human advantage. As antibiotic resistance increases interest in using bacteriophages to treat bacterial infections, understanding how phages generate variation — and how bacteria evolve resistance to them — could help researchers devise more effective phage therapies. Once again, practical science advances by studying mutation, selection and evolution, not by pretending that mutations are incapable of producing anything useful.
Here, then, is evolution reduced to its essentials and observed in the laboratory: replication errors arising without regard to what the phage needs, heritable variation among the resulting offspring, and an environment in which some variants reproduce more successfully than others. No foresight, planning or supernatural intervention is required — just mutation and natural selection.
The reversibility of these mutations is particularly instructive. A frameshift that is advantageous against TgvAB can be disadvantageous against McrA or McrBC, while another replication slip can restore the earlier form of the gene. Mutations are therefore not inherently beneficial or harmful, and evolution is not a march towards some predetermined ideal. Their effects depend on the environment in which their bearers must survive.
Dismissing the agt mutations as a “loss of information” merely defines the evidence away. When an altered DNA sequence gives its descendants a heritable ability to survive a defence that destroys other phages, biologically significant variation has plainly been produced. More importantly, natural selection has preserved contingency loci precisely because their instability enables phage populations to maintain alternative solutions to changing problems.
As for intelligent design, the supposed designer has equipped bacteria with elaborate mechanisms for destroying phages, equipped phages with mechanisms for defeating those defences, and left both sides locked in a perpetual evolutionary arms race. That is not evidence of benevolent planning; it is exactly the wasteful, opportunistic and endlessly shifting outcome expected from competing replicators subject to natural selection. Significantly, the researchers needed no creationist notion of “information”, no supernatural intervention and no magic creation event to explain their results. They used evolutionary theory to formulate their questions, interpret their observations and identify a mechanism that may eventually help medicine keep pace with antibiotic-resistant bacteria.
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