Hijacking Good Science: Lenski’s Bacteria Support Creation


Dr. Richard Lenski’s long-term evolution experiment with E. coli is commonly used to support evolution without distinction between observable limited change and unobservable molecules-to-man evolution. Many publications in scientific journals have described the mutations that have provided these bacteria with a benefit in their laboratory environment. A close look at the biochemical basis behind these mutations shows that the vast majority of fitness benefits are due to the disruption, degradation, or loss of unique genetic information. Furthermore, mutations that result in a gain of novel information have not been observed. As the idea of evolution from a simple, common ancestor requires the accumulation of novel genetic information over a long period of time, Lenski’s experiment then actually provides evidence against this idea and instead supports a Biblical creation model of life and origins.


The word evolution has been hijacked.  It is being used for both observable changes and unobservable changes.

This obfuscation was one of Ken Ham’s important points during the famous debate that occurred between him and Bill Nye.   When discussing evolution a distinction must be made between the observable process of natural selection and the unobservable idea of molecules-to-man evolution.  The kind of limited change that we can (and repeatedly) see is when natural selection (and other mechanisms) leads to variation within the originally created kinds. On the other hand, the unobservable idea of molecules-to-man evolution purports that small changes building up over a lengthy period of time has brought about the current biosphere from a common, simple ancestor.

Lenski’s long-term evolution experiment has been especially focused upon and cited by secularists in support of evolution.  Unfortunately, the distinction between observable variation and the unobservable idea of molecules-to-man evolution is rarely upheld.  However, a close look at the experiment actually provides evidence against molecules-to-man evolution and instead supports a biblical creation model of life and origins. 

The Experiment

Dr. Richard E. Lenski is an evolutionary biologist widely recognized for his long-term evolution experiment where several populations of Escherichia coli (E. coli) bacteria have been adapting to laboratory media for over 60,000 generations.  Though fitness gains decelerated after rapid increases within the first few thousand generations, an especially large fitness increase was observed when some E. coli populations evolved a “key innovation.” It is this moment in particular that captures the attention of many molecules-to-man evolution proponents so it is important for Christians to have a good understanding of the experiment in order that we may defend and demonstrate the truth of God’s Word through its findings. I hope to provide such information in what follows.

Lenski’s experiment demonstrates that the vast majority of fitness benefits are actually due to the disruption, degradation, or loss of genetic information

To investigate the experiment I reviewed 26 peer-reviewed, scientific articles authored by Dr. Lenski et al. published between 1991–2012 (see footnotes 1–16; 18–27). I was especially interested in papers that discussed the genetic changes in the E. coli populations as they adapted to their environment.  This is far from an exhaustive review; however, these papers represent the major genetic findings from over 20 years of the experiment.


The publications allege that several genes underwent a genetic mutation that conferred a benefit to the bacteria.  In no particular order, I will review each of these examples and discuss the known or hypothesized biochemical basis of how this benefit was achieved.  The scientific jargon may be confusing, but take special note of any trends regarding the mechanism of these changes.

  1. First is the pykF gene.  This gene encodes one of two pyruvate kinase enzymes that catalyzes the transfer of a phosphate group from phosphoenolpyruvate (PEP) to adenosine diphosphate (ADP) yielding a molecule of adenosine triphosphate (ATP).  PEP is also used to help drive the uptake of glucose, a limited energy source in the experiment.  The researches noted an insertion in this genetic region that they hypothesized to have inactivated this gene leading to a greater amount of PEP available to drive glucose uptake.9,16
  2. Second was an insertion mutation in the regulatory region of the pbpA-rodA operon.  This operon (which is a cluster of genes under the control of a similar regulatory unit) encodes two important proteins involved with cell wall synthesis.  As all 12 E. coli populations evolved larger cell volumes, the authors hypothesized that altered cell wall synthesis or timing of synthesis may have been beneficial.9,16 The exact mechanism of this mutation regarding a gain or loss of novel information is unknown. 
  3. A single nucleotide polymorphism (SNP) mutation was found in the mutS gene.  This SNP produced a premature stop codon and truncated the MutS protein leading to a defect in DNA repair.  This particular mutation was of importance because it greatly increases the number of mutations a bacterial population will accumulate over time.21,27
  4. The hokB-sokB gene locus in E. coli is a toxin-antitoxin system. When found in bacterial chromosomes, these systems are commonly involved in responding to stresses and bringing about programmed cell death.  The authors hypothesized that the observed insertion mutation would have knocked out this gene, and a disruption of hokB/sokB would likely be beneficial in the experimental environment.9,16
  5. The researchers observed that all 12 populations of E. coli lost the ability to catabolize D-ribose, an energy source that was not available in this experimental environment.  Furthermore, this loss of function was remarkably quick—within 2,000 generations all populations had lost the ability.  It was noted that this loss was caused by deletion mutations in the rbs operon.11,15  Interestingly, ribose is one of the energy sources that commensal E. coli use in the intestine. 
  6. DNA coiling is an important factor in gene regulation. and a mutation was found in the topA gene that encodes an enzyme that relaxes DNA coils.  Along with this, a mutation was found in the genetic region upstream of the fis gene.  The product of fis reduces activity of DNA gyrase which itself increases DNA supercoiling.  A loss or decrease of function in the protein products of both the topA and fis genes would contribute to the observed increase in DNA supercoiling.14,15
  7. The researchers found a small insertion mutation upstream of glmUS, an operon involved in cell wall biosynthesis.  It was hypothesized that this mutation inhibited normal binding of a transcriptional activator to this region thereby reducing glmUS expression.23 
  8. The nadR gene encodes a bi-functional protein involved in aspects of nicotinamide adenine dinucleotide (NAD) metabolism.  Specifically, this protein represses several genes involved in NAD synthesis so a disruption of this gene and its corresponding protein, especially the repressor function of the protein, would result in more NAD.  Dr. Lenski and colleagues observed an insertion mutation into the nadR gene and hypothesized that an increased intracellular concentration of NAD may be beneficial in this environment.9,16  This increase in NAD would be due to a loss of function in the repressor component of the protein.  
  9. Dr. Lenski and colleagues noted a mutation in spoT, the product of which is involved in the stringent response through a cell signaling molecule (ppGpp).  The precise physiological basis for this advantage is unknown; however no two mutations were identical among bacterial populations that evolved a mutation in this gene.12,15  This finding suggests that any fitness benefits from these mutations were due to a disruption of function.   
  10. Interestingly, many bacterial populations evolved resistance to a certain virus even though they were not exposed to that virus throughout the experiment.  The protein that the bacteria use to transport and metabolize maltose, an energy source that was not present in their experimental environment, is the same protein that the virus targets to infect the bacteria.  Since there is no maltose in the growth media, downregulating this unused metabolic pathway would be beneficial for the bacteria and just so happens to confer viral resistance as well.  Genetically this change resulted from a mutation in the malT gene, the regulator of maltose metabolism through positive regulation of the LamB surface protein.  Mutation in malT likely rendered its protein product nonfunctional thereby eliminating expression of LamB.24  
  11. Perhaps the most famous of all observations in Dr. Lenski’s long-term evolution experiment was when an E. coli population began to utilize a new energy source (citrate) that they normally could not use under aerobic conditions.  It is important to note that E. coli already have the ability to transport and metabolize citrate, but the bacteria typically cannot do so in oxic conditions as it does not produce an appropriate transporter in this type of environment (among other required factors).  The genetic changes that underlie this particular adaptation are complex, but a key event involved the replication of a genomic region that regulates a citrate transporter.  This amplification captured a previously existing and aerobically expressed promoter (the promoter for rnk) which could then direct transcription of the citrate transporter (citT).  Repeated tandem amplifications refined this function.27  

Putting It Together

The unobservable idea of molecules-to-man evolution hypothesizes that all living things have been derived from a common, simple ancestor in our distant past.  This would require the accumulation of novel information over a long period of time through genetic mutations.  However, Lenski’s experiment demonstrates that the vast majority of fitness benefits are actually due to the disruption, degradation, or loss of genetic information.  A possible exception to this tendency is the evolution of citrate utilization in aerobic conditions; however, no novel information was gained in this instance as this ability was the result of previously existing information being rearranged and used in a different way.  The novelty here was that no one had ever observed a promoter capture event for a gene involved in central metabolism.

It must be remembered that fitness improvements or even gains of protein function are not equivalent to a gain of novel information (GONI).  A loss of information occurring in a regulatory region may improve gene product function by increasing its expression, but this would not represent a GONI.  Neither would a mutation that brings back a function that was previously lost, a decrease in specificity of a protein’s function, a rearrangement of already existing information, the duplication of existing information, or the general increase in diversity over time.  A GONI must involve a mutational event or series of events that enable the production of novel protein(s) that can perform a specific and previously unknown activity.  This type of mutation has not been observed. 

Findings from this experiment demonstrate that the vast majority of adaptations are due to the loss of unique genetic information.  This is utterly opposed to the requirements of molecules-to-man evolution and is why Lenski’s experiment actually provides evidence against the truth of this idea.   

In the biblical creation model, God created various kinds of living organisms in a highly complex state.  Ever since the Fall of man in Genesis 3, genetic mutations have resulted in the degradation of information that, while having many negative consequences, come with the positive benefit of allowing populations to diversify and adapt to their new environments. When defending the truth of creation, we must remember that natural selection only exists due to the entrance of death into the world through sin (Romans 5:12) and proclaim that our only hope of salvation from sin and death is Jesus Christ. 

Answers in Depth

2014 Volume 9


  1. Lenski, R., M. Rose, S. Simpson, and S. Tadler. 1991. Long-term experimental evolution in Escherichia coli I. Adaptation and divergence during 2,000 generations. American Naturalist 138, no. 6:1315–1341.
  2. Lenski, R. and M. Travisano. 1994. Dynamics of adaptation and diversification: a 10,000-generation experiment with bacterial populations. PNAS 91:6808–6814.
  3. Travisano, M., J. Mongold, A. Bennett, and R. Lenski. 1995. Experimental tests of the roles of adaptation, chance, and history in evolution. Science 267, no. 5194:87–90.
  4. Travisano, M. and R. Lenski. 1996. Long-term experimental evolution in Escherichia coli IV. Targets of selection and the specificity of adaptation. Genetics 143, no. 1:15–26.
  5. Elena, S. and R. Lenski. 1997. Long-term experimental evolution in Escherichia coli VII. Mechanisms maintaining genetic variability within populations. Evolution 51, no. 4:1058–1067.
  6. Sniegowski, P., P. Gerrish, and R. Lenski. 1997. Evolution of high mutation rates in experimental population of E. coli. Nature 387:703–705.
  7. Arjan, J., M. de Visser, C. Zeyl, P. Gerrish, J. Blanchard, R. Lenski. 1999. Diminishing returns from mutation supply rate in asexual populations. Science 283:404–406.
  8. Cooper, V. and R. Lenski. 2000. The population genetics of ecological specialization in evolving Escherichia coli populations. Nature 407:736–739.
  9. Schneider, D., E. Duperchy, E. Coursang, R. Lenski, and M. Blot. 2000. Long-term experimental evolution in Escherichia coli IX. Characterization of insertion sequence-mediated mutations and rearrangements. Genetics 156:477–488.
  10. Cooper, V., A. Bennet, and R. Lenski. 2001. Evolution of thermal dependence of growth rate of Escherichia colipopulations during 20,000 generations in a constant environment. Evolution 55, no. 5:889–896.
  11. Cooper, V., D. Schneider, M. Blot, and R. Lenski. 2001. Mechanisms causing rapid and parallel losses of ribose catabolism in evolving populations of Escherichia coli B. Journal of Bacteriology 183, no. 9:2834–2841.
  12. Cooper, T., D. Rozen, and R. Lenski. 2003. Parallel changes in gene expression after 20,000 generations of evolution in Escherichia coli. PNAS 100, no. 3:1072–1077.
  13. Lenski, R., C. Winkworth, and M. Riley. 2003. Rates of DNA sequence evolution in experimental populations of Escherichia coli during 20,000 generations. Journal of Molecular Evolution 56:498–508.
  14. Crozat, E., N. Philippe, R. Lenski, J. Geiselmann, and D. Schneider. 2005. Long-term experimental evolution in Escherichia coli XII. DNA topology as a key target of selection. Genetics 169:523–532.
  15. Pelosi , L., L. Kühn, D. Guetta , J. Garin, J. Geiselmann, R. Lenski, and D. Schneider. 2006. Parallel changes in global protein profiles during long-term experimental evolution in Escherichia coli. Genetics 173:1851–1869.
  16. Woods, R., D. Schneider, C. Winkworth, M. Riley, and R. Lenski. 2006. Tests of parallel molecular evolution in a long-term experiment with Escherichia coli. PNAS 103, no. 24:9107–9112.
  17. Bergthorsson, U., D. Andersson, and J. Roth. 2007. Ohno’s dilemma: evolution of new genes under continuous selection. PNAS 104, no. 43:17004–17009.
  18. Blount, Z., C. Borland, and R. Lenski. 2008. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. PNAS 105, no. 23:7899–7906.
  19. Sleight, S., C. Orlic, D. Schneidert, R. Lenski. 2008. Genetic basis of evolutionary adaptation by Escherichia coli to stressful cycles of freezing, thawing and growth. Genetics 180:431–443.
  20. Barrick, J. and R. Lenski. 2009. Genome-wide mutational diversity in an evolving population of Escherichia coli. Cold Spring Harbor Symposia on Quantitative Biology 74:119–129.
  21. Barrick, J., D. Yu, S. Yoon, H. Jeong, T. Oh, D. Schneider, R. Lenski, and J. Kim. 2009. Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature 461:1243–1247.
  22. Rozen, D., N. Philippe, J. Arjan de Visser J, R. Lenski, and D. Schneider. 2009. Death and cannibalism in a seasonal environment facilitate bacterial coexistence. Ecology Letters 12:34–44.
  23. Stanek, M., T. Cooper, and R. Lenski. 2009. Identification and dynamics of a beneficial mutation in a long-term evolution experiment with Escherichia coli. BMC Evolutionary Biology 9:302.
  24. Meyer, J., A. Agrawal, R. Quick, D. Dobias, D. Schneider, and R. Lenski. 2010. Parallel changes in host resistance to viral infection during 45,000 generations of relaxed selection. Evolution 64:3024–3034.
  25. Wielgoss, S., J. Barrick, O. Tenaillon, S. Cruveiller, B. Chane-Woon-Ming, C. Médigue, R. Lenski, and D. Schneider. 2011. Mutation rate inferred from synonymous substitutions in a long-term evolution experiment with Escherichia coli. G3 1:183–186.
  26. Woods, R., J. Barrick, T. Cooper, U. Shrestha, M. Kauth, and R. Lenski. 2011. Second-order selection for evolvability in a large Escherichia colipopulation. Science 331:1433–1436.
  27. Blount, Z., J. Barrick, C. Davidson, R. Lenski. 2012. Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature 489:513–518.


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