Orphan genes are the hard problem for evolutionary genomics

Challenging LUCA: A Critical Examination of Evolutionary Claims

The theory of a Last Universal Common Ancestor (LUCA) posits that all life on Earth shares a single, ancient origin. This concept forms a cornerstone of modern evolutionary theory. However, several lines of evidence challenge the notion of a singular, linear progression of life from a common ancestor. Specifically, the C-value paradox, the existence of orphan genes, and the nature of pseudogenes collectively undermine the simplicity and plausibility of the LUCA hypothesis.

The C-Value Paradox

One of the most perplexing challenges to the LUCA concept is the C-value paradox, which describes the lack of correlation between an organism’s genome size (C-value) and its perceived complexity. If all life descended from a common ancestor, one would expect a more straightforward relationship between genome size and organismal complexity. Yet, this is not observed. For instance, the human genome contains approximately 3 billion base pairs, while the genome of the amoeba Amoeba dubia exceeds 600 billion base pairs, despite the amoeba being a single-celled organism.

This paradox suggests that genome size is influenced by factors other than just the accumulation of beneficial mutations. The presence of large amounts of non-coding DNA, repetitive sequences, and other genomic elements that do not contribute directly to organismal complexity indicates that genome change is driven by complex mechanisms beyond natural selection. This complexity is inconsistent with the gradual, stepwise progression expected from a LUCA-based evolutionary model.

Orphan Genes

Orphan genes, also known as de novo genes, present another significant challenge to the LUCA hypothesis. These genes lack recognizable homologs in other species and appear to be unique to particular lineages. Their sudden appearance without any apparent ancestral sequence contradicts the gradualist narrative of evolutionary theory.

For example, a study on fruit flies (Drosophila) identified numerous orphan genes that are species-specific and do not show any similarity to genes in closely related species. These genes often play crucial roles in the unique biological functions and adaptations of the organisms that possess them. The existence of orphan genes suggests the presence of mechanisms capable of generating entirely new genetic sequences independently of common descent, which aligns more closely with an intelligent design and Creation perspective than with the slow, incremental changes posited by LUCA.

https://communities.springernature.com/posts/the-evolutionary-mystery-of-orphan-genes

"Orphan genes are "the hard problem" for evolutionary genomics. Because we can't find other genes similar to them in other species, we can't build family trees for them. We cannot hypothesise their gradual evolution; instead they seem to appear out of nowhere. Various attempts have been made at explaining their origins but – as Paul and I describe in our book chapter – the problem remains unsolved.

Give their ubiquity in all genome sequences orphan genes receive comparatively little attention from the research community. I suspect this is partly because they are such a difficult problem. Science is "the art of the soluble". It may be that little funding finds its way to the origin of orphan genes because it appears to be an insoluble problem."

Pseudogenes

Pseudogenes, or non-functional sequences resembling functional genes, have traditionally been cited as evidence for common ancestry due to their presumed role as evolutionary relics. However, recent research has revealed that many pseudogenes are not merely "junk" DNA but have regulatory functions, influencing the expression of other genes and playing roles in genetic networks.

For instance, some pseudogenes are involved in gene regulation during development, acting as decoys for regulatory molecules or producing non-coding RNAs that influence gene expression. This functional versatility indicates that pseudogenes are integral components of the genome, not vestigial remnants of an evolutionary past. Their existence and function challenge the idea that genomes are solely shaped by random mutations and natural selection from a common ancestor.

The Role of CpG Islands

CpG islands are regions of DNA where a cytosine nucleotide occurs next to a guanine nucleotide in the linear sequence of bases. These regions are crucial for gene regulation. However, the methylation of cytosines within CpG sites can lead to their deamination and conversion into thymine, causing mutations. Over time, this process leads to the inevitable depletion of CpG islands. Importantly, cells lack a mechanism to regenerate CpG islands once they are lost, making this a one-way path to degradation. This inevitable breakdown challenges the idea that complex genomes can be maintained through natural processes alone, casting further doubt on the LUCA hypothesis.

Alternative Explanations and Intelligent Design

The intricate mechanisms governing genome size, the emergence of orphan genes, the functional complexity of pseudogenes, and the degradation of CpG islands suggest a level of complexity that is difficult to reconcile with the LUCA model. Instead, these observations are more consistent with the idea of an intelligent design, where genomes are seen as dynamic, information-rich systems capable of rapid adaptation and innovation.

Moreover, the presence of sophisticated genetic mechanisms that can compensate for gene loss or alter gene expression patterns underscores the notion of a designed adaptability in living organisms. For example, alternative splicing mechanisms enable cells to produce multiple protein variants from a single gene, demonstrating an inherent flexibility and robustness in the genetic code that surpasses simple evolutionary explanations.

Conclusion

While the concept of a Last Universal Common Ancestor remains a central tenet of evolutionary theory, numerous empirical observations challenge its validity. The C-value paradox, orphan genes, the functional complexity of pseudogenes, and the inevitable breakdown of CpG islands suggest a more intricate and intelligently orchestrated biological landscape. These findings invite a reconsideration of the origins and mechanisms of life, emphasizing the need for alternative frameworks that account for the observed genetic diversity and complexity.

There is no mechanism for evolution. Observed science points to Intelligent Design and Creation.

References

1. Gregory, T. R. (2005). The C-value enigma in plants and animals: a review of parallels and an appeal for partnership. Annals of Botany, 95(1), 133-146.
2. Tautz, D., & Domazet-Lošo, T. (2011). The evolutionary origin of orphan genes. Nature Reviews Genetics, 12(10), 692-702.
3. Poliseno, L., et al. (2010). A coding-independent function of gene and pseudogene mRNAs regulates tumour biology. Nature, 465(7301), 1033-1038.
4. Bird, A. (1986). CpG-rich islands and the function of DNA methylation. Nature, 321(6067), 209-213.