Cowards die many times before their deaths; The valiant never taste of death but once.
(Julius Caesar, 2.2.32–37)
New work by researchers from Great Britain reveals that mutation rates in the genome of E. coli are nonrandom and optimized to minimize their impact on survival. This optimization adds to the case for intelligent design. Moreover, it challenges a key assumption made by evolutionary biologists, namely that shared DNA sequences in the genome of related organisms serves as evidence for common descent and, consequently, biological evolution.
They say death and taxes are the only two things certain in life. But in biology, there is a third inevitability: mutations. Changes will happen in an organism’s genetic material and, as a result, the DNA sequences of the genome will be altered.
Although evolutionary biologists regard mutations as the engine that drives the evolutionary process, more often than not, mutations are deleterious to the organism. These scientists have long thought that mutations occur in genomes randomly. Natural selection fixes into the population the few mutations that increase the organism’s fitness. But a recent study indicates that organisms can manage mutations, much in the same way an accountant structures finances to reduce the amount of taxes a client owes.
This newly recognized ability challenges one of the key assumptions evolutionary biologists employ when interpreting genomes’ shared features as evidence for common descent and, hence, biological evolution. On the other hand, this discovery can be rightly enlisted to further the case for intelligent design.
Nonrandom Mutations in E. coli
By analyzing and comparing the genomes of 30 E. coli strains, researchers from Great Britain discovered that the mutation frequency varies across this bacterium’s genome.1 Some regions (hot spots) have a relatively high mutation rate; others (cold spots) display a relatively low rate of genetic change.
The researchers learned that hot and cold spot locations are not random. Hot spots occur in regions where mutations would do the least amount of damage. Meanwhile, cold spots show up in areas that harbor genes critical for E. coli’s survival. The hot and cold regions both typically encompass large stretches containing genes that are part of the same operon. These neighboring genes often encode proteins that participate in the same cellular processes.
Additionally, the researchers determined that cold spots tend to occur in highly expressed genes. Yet because transcription (which dictates, in part, the rate of gene expression) tends to cause mutations, it seems that hot spots should associate with highly expressed genes. This surprising result indicated to the investigators that there must be some mechanism that actively manages the mutation rate, compensating for the transcriptional process’s mutagenicity.
Thus, it appears that the mutation rates across genomes have been optimized to reduce the risk of harmful genetic changes. Although the nonrandom distribution of mutations in genomes is contrary to the most common understanding of evolutionary theory, it is not surprising to learn that mutation rates and the location of mutational hot and cold spots are optimized to protect E. coli from the loss of fitness. Biochemical systems are characteristically optimized. (For more examples of such optimization, visit these previous articles on metabolism, amino acids, the genetic code, and synonymous codons.) It is reasonable to think that, if mutation rates across the E. coli genome have been optimized to minimize damaging effects, then the rates are optimized similarly in other organisms’ genomes.
This result is consistent with research that demonstrates that substitution mutations and recombination are nonrandom and take place in hotspots. Other studies also show that other genome-altering processes (such as intron insertion and transposon insertion) are nonrandom, occurring in hot spots, as well.
Nonrandom Mutations and the Case for Design
As I discussed in my book The Cell’s Design, the characteristic features of life’s chemistry are the same as what we would recognize as evidence for a human designer’s work. So, by analogy, it is logical to conclude that a Mind was responsible for bringing life into existence. Systems, objects, devices, etc., designed by humans are often optimized. In fact, optimization connotes high quality and superior designs. As such, the optimization of mutation rates can be seen as further evidence for intelligent design in nature. The distribution of hot and cold spots across the genome and association of cold spots with genes critical for survival portrays an elegance and cleverness that bespeaks of a Creator’s handiwork.
Nonrandom mutation rates also raise questions about the validity of a key assumption made by evolutionary biologists when they interpret shared features of genomes as evidence for common descent.
The Challenge for Biological Evolution
Evolutionary biologists consider identical (or nearly identical) DNA sequence patterns found in the genomes of related organisms as evidence of descent from a shared ancestor. According to this line of reasoning, the shared patterns arose as a result of mutational events that occurred in the common ancestor’s genome. Presumably, as the varying evolutionary lineages diverged from the nexus point, they carried with them the altered sequences created by the primordial mutations. This interpretation rests on the underlying assumption that the mutations that generated the shared fingerprint are rare and random.
But, if the mutations are nonrandom—preferentially taking place in hot spots—then it could be asserted that the DNA sequence patterns were generated independently in the separate biological groups. That is, the shared DNA sequence patterns may not be the result of descent with modification from a common ancestor, but instead arose separately. In other words, shared DNA sequences are not necessarily evidence for common descent and biological evolution.
Death and taxes may be a given, but the case for biological evolution is far from certain.
- Iñigo Martincorena, Aswin S. N. Seshasayee, and Nicholas M. Luscombe, “Evidence of Non-random Mutation Rates Suggests an Evolutionary Risk Management Strategy,” Nature 485 (May 3, 2012): 95–98, http://www.nature.com/nature/journal/v485/n7396/full/nature10995.html.