Evolutionary problems with orphan genes.

With the discovery that DNA possesses duplicate strands hiding a coded message, many thought that the mechanism of biological evolution would be proven through the inheritance of this molecule from generation to generation. We are still waiting for a genuine mechanism for evolution to be discovered so that the theory makes sense.  Seventy years later, the massive amount of sequencing of genomes that was supposed to support the “tree of life”, so easily and seductively drawn by evolutionary biologists, has failed to do so.  The tree had to be abandoned since sequencing can align almost any being with another being.  Still, the theory has not been abandoned and many neat little imaginative stories are told and retold and modified to explain what has been found in the coded message of DNA.



Thousands of gene sequences and their controlling sequences have been analyzed.  Genes that code for proteins which share some functional attributes also share similar sequences.  Whole families of genes have been cataloged.  Some have the superficial appearance of being composed of chunks of other genes.  These genes are thought to produce proteins with sequences or “domains” that mirror the function of similar proteins.  Many of these gene families are found throughout the living world.

For instance, all cells possess ribosomes; the macromolecular machine that knits proteins into existence based upon the genetic message.  Both the RNA frame of ribosomes and the 70-100 proteins that assemble into the functional machinery that makes the ribosome share homologies (sequence identity) throughout living things.  Though the bacterium E. coli has a ribosomal protein L9 for its ribosome, the L9 protein in humans has a different sequence with shared similarities to the bacterial protein.  Other proteins have shared sequences for binding calcium.  Some proteins bind calcium to activate respiration, other proteins bind calcium to activate gene expression and still, other proteins bind calcium to buffer the calcium concentration.  Calcium binding proteins are a large family. Also, most of the proteins that do the work of general metabolism are considered “homologous” in all cellular life forms.  While they may be vastly different in terms of identical sequences, large tracts of “similar” sequences are shared.




These findings were considered to be evidence that evolution does not have to start with completely novel DNA sequences to create a new gene.  In this way, genes are thought to have been duplicated in the genome then modified by mutation over time or altered by natural gene splicing to give rise to brand new sequence combinations that do some new but similar biochemistry or some very novel biochemistry in the cell.  Thus, theories of the common ancestry of whole families of genes have been used to support the idea of molecular evolution.

Only circumstantial evidence exists that such swapping of chunks of DNA, or gene duplication/mutation has occurred to produce new genetic information.  No one has seen this happen.  It is assumed to have occurred since the reality that 23000 genes in the human genome could not have arisen de novo from the chaos of mutation and selection, given the circumstances of the age of the universe and the earth in particular.  The statistical probabilities against this happening are staggering.




As genomes are sequenced, protein coding regions are recognized by a number sequence attributes that are common to genes that are known to code for functional proteins.   Typically, sequences of DNA that are longer than 100 base pairs as determined by the presence of a start code – ATG- and followed by a stop codon -TAG- are labeled as open reading frames or ORFs. This notation makes the discovery and recording of potentially new functional genes much easier than other methods of discovery.  Though a reliable and useful method for finding the placement of known gene sequences in a particular genome, it has also given evidence of a startling impasse for theoretical biological evolution.


A vast array of genes are being found that are so unique as to have absolutely no similarity to existing gene sequences either within the species or between species.  In other words, the genes are not similar to other genes in that particular genome or in any other genome.  In fact, 10 to 40% of genes discovered are considered to be orphan genes.  They are orphaned because they seem to have no apparent evolutionary parentage.  That is, they have no similarity, no homology and no shared domains to other genes.  And these genes are bound to species in which they are found.  In the case of the ant, 28,581 genes are found to be unique only to ants and not found in other insects. Within seven species of ants, only 64 genes were common to all seven ant species.



Between chimpanzees and humans, over 1177 genes have been discovered so far as ORFs (open reading frames or potential gene sequences) and exist only in the species, Homo sapiens or the chimpanzee; but not both. Because this is troubling to evolutionary biology, the genes have been scrubbed from gene databases until it can be proven that these gene sequences do code for functional proteins.




“The remaining 1,177 cases were declared to be orphans, because they lack orthology, paralogy, or homology to known genes and are not obvious artifacts… If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes… We found… 12 reported cases of orphans with experimental evidence for an encoded protein”[1].


When evidence doesn’t support the paradigm of evolution it is not used to correct the theory but is tossed out until further notice.  This is not science.  It is ignorance.

A better premise for the evidence is that orphan genes are what makes a species unique.  And this should hold until proven otherwise.


For more on orphan genes go to: http://www.icr.org/article/9145/282


  1.  Clamp M, Fry B, Kamal M, Xie X, Cuff J, Lin MF, Kellis M, Lindblad-Toh K, Lander ES.Distinguishing protein-coding and noncoding genes in the human genome. Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19428-33. Epub 2007 Nov 26. PubMed PMID: 18040051; PubMed Central PMCID: PMC2148306.

2 Responses to “Evolutionary problems with orphan genes.”

  1. Nathan M.


    I found this comment:

    “Seventy years later, the massive amount of sequencing of genomes that was supposed to support the “tree of life”, so easily and seductively drawn by evolutionary biologists, has failed to do so. The tree had to be abandoned since sequencing can align almost any being with another being.”

    most interesting. Interesting in that it seems to be pure assertion, and nothing more. What tree had to be abandoned? What is your evidence that “sequencing can align almost any being with another being”? You say you are a molecular biologist, but how could a molecular biologist write something so devoid of evidence and expect anyone to believe it? Is this an example of what you wrote in a comment on Ed Yong’s Discover Magazine blog entry about ENCODE back in 2012:

    “Truth in sequencing and freedom of interpretation are hallmarks of great science.”

    Do you think all interpretations are equally valid? It seems so. About 16 years ago, Paul Nelson declared on a discussion forum that molecular phylogenetics (what you are referring to above) was unreliable because of researcher bias, that people could align things the way they wanted to. I was working on the phylogeny of 30+ species of primate at the time. I removed any indication of what they were, removed all gaps, and altered their order and sent him a FASTA file and a link to a list of free phylogenetics alignment and analysis packages, and asked him to support his claim. If what he claimed were true, then his analysis should produce a very different alignment and phylogeny than mine. He, of course, declined.

    So, when you write “sequencing can align almost any being with another being”, I suspect you are in the same boat as Nelson, for the data used and information found at these sites:



    and hundreds of publications does not seem to bear your unsupported assertion out very well.

    In that blog comment in 2012, you also wrote:

    “Even transposons which currently seem to have no activity will prove to be vital not viral as we learn more about control and development.”

    So, how is that coming?

    • Dr. Daniel Moran, Ph.D.

      It appears you have not followed the argument as the post surrounds the admission by advocates of molecular phylogeny that the game is fixed and unable to reproduce the tree of life. So, if you find me incredible, you find other scientists, and secular at that, even more incredible.

      It seems you are not familiar with the lack of evidence that transposons in the human genome are of very little homology to viral elements. The so poor are the alignments that it appears to clearly be a best guess since no one has found a function to the elements otherwise. However, the encode project is asserting that 80% of the human genome is functional and as more information is coming in it appears that number will rise to over 100% as information is found running both strands of DNA, overlapping regions of known function. Transpososons appear to have regulatory function and do not appear to be “transposable.”

      It is incredible that one who asserts such skill in the science of bio information does not really understand what he or she is looking at… information does not arise from chaos or accident. Intrinsically, humans know this from a very early age, and your lack of understanding shows how well indoctrinated you are in the science of your religion.


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