A few days ago, I discussed a recent study that revealed the mutation rates in the E. coli genome are not random as expected by the evolutionary paradigm. Rather, these rates are nonrandom and optimized to minimize the deleterious effects of mutations. Mutational hot spots occur in regions of the genome that (1) encode for processes not critical for cell survival; (2) harbor genes expressed at low levels; and (3) specify rarely used metabolic processes.
Still, mutations do happen. And according to evolutionists, these genetic changes drive the evolutionary process. Natural selection eliminates harmful mutations from the gene pool. However, advantageous changes can lead to new biochemical function and increased fitness.
I am skeptical about the ability of chemical evolution and macroevolution to account for life’s origin and history. (See Origins of Life, Creating Life in the Lab, and What Darwin Didn’t Know for detailed discussions about the scientific problems with chemical evolution and macroevolution.) However, I am convinced that some forms of evolution are valid, namely: microevolution, speciation, and microbial evolution.
For example, ample evidence exists that bacteria evolve. The Long-Term Evolution Experiment (LTEE), conducted by scientists from Michigan State University, demonstrates this point.
The Long-Term Evolution Experiment
Inaugurated in 1988 and led by Richard Lenski, this study was designed to monitor evolutionary changes in E. coli. The LTEE began with a single cell of E. coli that was used to generate twelve genetically identical lines of cells.
The twelve clones were inoculated separately into a minimal growth medium that contained low levels of glucose as the only carbon source. After growing overnight, an aliquot of each culture was transferred into fresh growth media. This process has been repeated every day for about twenty years. Throughout the experiment, aliquots of cells have been frozen every 500 generations. These frozen cells represent a “fossil record” of sorts that can be thawed out and compared to current and other past generations.
The forces of natural selection have been controlled carefully in this experiment. Temperature, pH, nutrients, and oxygen exposure have remained constant for the last twenty years. Starvation is the primary challenge facing these cells.
E. coli grown under aerobic (oxygen-based) conditions can’t use citrate as a food stuff. This bacterium has the biochemical machinery to metabolize citrate; it just can’t transport the compound across its cell envelope. But, in the absence of oxygen, E. colican transport citrate into the cell and utilize it as a carbon source.
The research team has taken advantage of E. coli’s deficiency to monitor for contamination in their experiment. They added citrate at relatively high levels to the growth media. Since other microbes can typically make use of citrate, any contaminating microbe accidently introduced during the transfer steps will grow to greater cell densities than E. coli, causing the media to turn cloudy.
The Evolution of Citrate Utilization
Around 32,000 generations into the LTEE, E. coli started utilizing citrate as a carbon source. The team reasoned that this newly acquired ability resulted from a series of mutations to the E. coli genome.
New work from Lenski’s laboratory has identified, at least in part, the changes that led to E. coli’s ability to transport citrate into the cell under aerobic conditions.1 It turns out that this new capability did not involve the evolution of a new gene, but the altered expression of the existing gene that encodes for a citrate transpoter. This gene is expressed when the cells are grown in the absence of oxygen. But the gene is not expressed under aerobic conditions.
The key change that led to the altered gene expression involved a genomic rearrangement in which regions of the genome were swapped. When this happened, a promoter that triggers the expression of a gene involved in energy metabolism under aerobic conditions became associated with the gene that encodes the citrate transporter. This means that the citrate transporter gene is now expressed under aerobic conditions.
While the genomic rearrangement was the principal event that led to citrate transport in the presence of oxygen, it was not the only change involved in E. coli’s evolution. Two potentiating mutations to the genome were required before the rearrangement took place. The exact nature of these changes is still unknown—but they are required. If they do not take place, the genome shuffling will not lead to the ability to transport citrate into the cell under aerobic conditions.
One other step was necessary. This step took place after the citrate transporter captured the aerobic promoter sequence. It involved genome duplication events that yielded multiple copies of the citrate transporter (and newly associated promoter). The duplication caused the expression of the citrate transporter gene to become amplified.
Based on this remarkable work, it is clear that E. coli (and by extension, other bacteria) can evolve.
Validation for the Evolutionary Paradigm?
The fact that bacteria can evolve doesn’t mean that evolutionary processes can account for life’s origin and history. For a detailed discussion on this topic click on the links below:
- “Long-Term Evolution Experiment: Evidence for the Evolutionary Paradigm? Part 1 (of 2)”
- “Does the Evolution of Caffeine-Eating Bacteria Stimulate the Case for Biological Evolution?”
While many evolutionary biologists will point to studies like the LTEE as support for the evolutionary paradigm, this study has generated some unexpected results—results that, in my mind, challenge key ideas of biological evolution. Click on the links below to read a couple of articles on the problems the LTEE creates for the evolutionary model:
- “Inability to Repeat the Past Dooms Evolution”
- “Long-Term Evolution Experiment: Evidence for the Evolutionary Paradigm? Part 2 (of 2)”
- Zachary D. Blount et al., “Genomic Analysis of a Key Innovation in an Experimental Escherichia coli Population,” Nature 489 (September 27, 2012): 513–18.