Genetic Entropy: Evidence from Bacterial, Yeast, Drosophila, C. elegans, and Human Genetic Data
Introduction
Genetic entropy refers to the hypothesis that genomes are deteriorating over time due to the accumulation of deleterious mutations. This concept challenges the traditional evolutionary framework, which posits that natural selection and beneficial mutations drive the progressive complexity and adaptability of organisms. This article combines empirical evidence from various organismal experiments and human genetic data to illustrate the pervasive impact of genetic entropy.
Evidence from Organismal Experiments
Bacteria: A key study highlighting genetic entropy in bacteria comes from Richard Lenski’s Long-Term Evolution Experiment (LTEE) with Escherichia coli. Over 50,000 generations, the bacterial populations were observed to undergo significant genetic changes. Notably, a study published in 2016 revealed that these bacteria lost approximately 1.4% of their DNA, an indication of genetic deterioration over time. Today, after 90,000 generations, the bacteria have lost almost 3% of their DNA.
Yeast: Studies on yeast (Saccharomyces cerevisiae) have shown that over extended periods of replication, there is a noticeable decline in genetic stability. Accumulation of deleterious mutations in these populations has led to a decrease in overall fitness, demonstrating another clear example of genetic entropy.
Drosophila: Research on fruit flies (Drosophila melanogaster) has similarly indicated that long-term mutation accumulation experiments result in reduced viability and fitness. These studies consistently show a decline in the adaptive potential of populations, reinforcing the concept of genetic entropy.
C. elegans: Experiments with the nematode Caenorhabditis elegans have revealed that mutation accumulation can lead to significant declines in fitness and reproductive success. These findings support the hypothesis that genomes are subject to degradation over time due to the accumulation of harmful mutations.
Evidence from Human Genetic Data
The DisGeNet Plus database provides a comprehensive view of the human genome's susceptibility to deleterious mutations. Here are the key statistics from the latest version (v24.1):
- Gene-Disease Associations (GDAs): 1,793,304 associations between 26,090 genes and 39,797 diseases and traits.
- Variant-Disease Associations (VDAs): 1,201,698 associations between 704,086 variants and 16,774 diseases and traits.
- Disease-Disease Associations: Over 49 million associations.
- Animal Model Associations: Over 290,000 associations involving 12,000 diseases detected in animal models.
- Chemical Annotations: 3,981 chemicals associated with GDAs and VDAs.
- Publications Supporting Data: 1,470,167 publications for GDAs and 173,659 publications for VDAs, totaling 1,479,286 publications.
This data underscores the extensive presence of harmful mutations within the human genome, supporting the concept of genetic entropy.
Genetic Entropy: A Unified Perspective
Bacterial Genetic Deterioration:
- The LTEE demonstrates a clear example of genetic entropy. The observed DNA loss over generations indicates a net loss of genetic information, contradicting the expectation of evolutionary progress through beneficial mutations.
Yeast, Drosophila, and C. elegans Studies:
- Long-term studies on yeast, fruit flies, and nematodes all show a pattern of declining genetic stability and fitness due to mutation accumulation. These results are consistent with the concept of genetic entropy, where genomes degrade over time.
Human Genetic Burden:
- The vast number of gene-disease and variant-disease associations in humans points to a significant burden of deleterious mutations. The DisGeNet Plus data reveals that a large proportion of the human genome is implicated in various diseases, further supporting the concept of genetic entropy.
Conclusion
The combined evidence from bacterial, yeast, Drosophila, C. elegans, and human genetic data provides a compelling case for genetic entropy. The continuous accumulation of deleterious mutations and the loss of genetic information over time challenge the evolutionary paradigm and support the concept of a designed genome subject to decay post-fall. The DisGeNet Plus data on human diseases and genetic variants highlights the pervasive impact of harmful mutations, reinforcing the need for a re-evaluation of evolutionary assumptions.
References
- Maddamsetti, R., Lenski, R. E., & Barrick, J. E. (2016). Adaptation, Clonal Interference, and Frequency-Dependent Interactions in a Long-Term Evolution Experiment with Escherichia coli. Genome Biology and Evolution, 8(11), 3025–3034.
- DisGeNet Plus. (2024). Gene-Disease Associations Database. DisGeNet Plus.
- Lynch, M., & Walsh, B. (1998). Genetics and Analysis of Quantitative Traits. Sinauer.
- Denver, D. R., et al. (2004). High Mutation Rate and Predominantly Male-Biased Mutation in C. elegans. Nature, 430(7000), 679-682.
- Halligan, D. L., & Keightley, P. D. (2009). Spontaneous Mutation Accumulation Studies in Evolutionary Genetics. Annual Review of Ecology, Evolution, and Systematics, 40, 151-172.
