"Scientists long assumed that evolution made new genes from old ones - by copying them in error, or by fusing together or breaking apart existing ones. Now, more and more examples are emerging of genes being created 'de novo', from barren non-coding portions of the genome." ~ Adam Levy, Genes From The Junkyard
Introduction
The theory of evolution explains why we see the fossil record going from simple to complex over about 15,000 ft of sedimentary rock with scores of transitional fossils and no mixing over 500 million years. It explains the endemic biota of the Hawaiian Islands via biogeography and it’s geology including the Emperor Seamounts through a Pacific hot spot and plate tectonics. It explains why pterodactyls are only found in one layer and never with human remains or more ancient life forms. It explains crazy anatomical features like the recurrent laryngeal nerve in vertebrate necks, the inverted and poorly designed vertebrate eye with at least four workarounds by natural selection, and the finding of thousands of pseudogenes we share with other species - genes deactivated by mutations - including three for making egg yolk even though we don’t lay eggs. These and more examples are discussed in the blog on why intelligent design is only credible if one chooses to cherry pick nature, conflating complexity with design, and ignoring all the biology that tells us we are the product of evolution and not intelligent design. See blog on ID here.
For significantly new species to form it would take the ability of nature to produce new genes, new products that various selection forces could identify as important in survival and reproduction, and then promote them to spread in successive populations. Natural selection diminishes variation. Thus, this is a foundational need, and all “macroevolution” claims would fail if new genetic information, new genes could not arise. Gain of function is needed. Gain of information, however one wants to define “information”, genetically is especially required.
Setting the stage - the issue
For anti-evolutionists, the mantra that nature can’t produce new genes that make new information for evolution is a major assertion. As in the false claim proclaimed by many creationists that there are no transitional fossils - because to them there can’t be - they must claim there can never be new genes and no new information formed. Variation is limited to speciation from “kinds” because macroevolution is assumed impossible. It’s a presupposition that macroevolution has never happened despite DNA findings that essentially prove it.The variety in life to them originates like an orchard and not like a bush. Most creationists claim diversity and variety arises not from new genes but from the originally created genomes that supposedly carry enough diversity to only form similar species within limits; for example dog kind, cat kind, and humans were specially created without ape ancestors. This results in microevolution of “kinds” only - no evolution between major groups and certainly not human evolution from shared ancestors with the other great apes (but we now have the DNA findings to prove human evolution is true). See The Demise of Evolution Objections. This is the opposite of accepted evolution, and indeed Michael Behe in his book “Darwin Devolves” discusses example after example of genes that are turned off and disabled so new phenotypic changes can come about. His central point is that only previously present genes are disrupted to see the changes we observe, for example with polar bears degrading genes to match its diet and white fur. Behe writes in his third book, “Darwinian evolution proceeds mainly by damaging or breaking genes, which, counterintuitively, sometimes helps survival. In other words, the mechanism is powerfully devolutionary. It promotes the rapid loss of genetic information”(1). There is little to no room for the formation of new genes, new information for natural selection to work on in the anti-evolutionist world of species origins. Several scientists pointed out how wrong Behe is again. But is that true? Are there no examples of new genes forming? Have evolutionary biologists been fooled, or worse in denial? (17).
Methods for acquiring new genes
On the genetic level mutations are changes in the DNA letters of the genome. They can be beneficial or deleterious. Many people are under the impression that point mutations, changing a single letter of the ATCG letters in DNA, is the primary way mutations are proposed to occur and add new information to genomes but this is not the case. In the Origins of New Genes and Pseudogenes several ways new genes form are discussed (2).
1. Gene Duplication
Most evolutionary biologists would probably point out that new genes predominantly arise through gene duplications. Duplications are very common. Even today in our present human population, we have what are called copy variants between people. Finlay notes that genomic analysis has identified 11,700 variable locations in the human genome where any two people differ at about 1,100 of these DNA areas that are copied but not equally present in different people. Any two people vary by the number of olfactory receptor genes, and in a few taste receptor genes. It is true that people can taste and smell differently at least in part due simply to the number of receptor genes they have. We have little cellular factories for making proteins called ribosomes and people have from 35 to 175 copies of the rRNA genes. People vary by the number of salivary amylase genes they have, with European and Japanese populations having the higher number of AMY1 genes. The more salivary amylase you have the better at breaking down starches starting in your mouth and this will lessen the chance of developing diabetes (3).
The idea is that when genes are duplicated, most copies develop disabling mutations because the original gene is still present and the duplicated gene is not under strong selection to conserve it. Many would then become pseudogenised. But rarely, mutations develop that allow the copied gene to acquire the ability to make new products that can have new functions. Gene duplication rates are actually very high (2).
The platypus has venom in its spurs that includes three peptides similar to a compound it uses in its immune system with antimicrobial properties. It evolved from gene duplications (4). Opsin genes for color detection evolved from duplications (5).
In one experiment, scientists disabled a gene in Salmonella enterica that makes tryptophan. Another gene with a different function had a weak ability to do some of the original gene’s work. The bacteria duplicated the second over-worked gene and the copies acquired random mutations that eventually led to a second new different gene that evolved a new function making tryptophan again. This occurred in just a year and 3,000 generations (6).
A gene that codes a receptor for sialic acids underwent gene duplication to produce a new gene and the story has been revealed by scientific sleuths. “The SIGLEC11 gene was duplicated in an ancestor of humans and chimps…the duplicated copy was pseudogenised and part of the pseudogene subsequently pasted back into the parent SIGLEC11 gene… A subsequent gene conversation went the other way, generating a revivified allele of the pseudogene. The… process generated two novel genes existing only in humans. The novel SIGLEC11 gene encodes a protein with novel sialic acid-binding properties, and is expressed by microglial cells in the brain. It is also active in the ovary… and, when abnormally expressed, to a uniquely human disease (polycystic ovarian syndrome)” (3).
Work by Nathan Lents and students discovered that some microRNA genes found on human chromosome 21 were not found in the other great apes. These in the past might be considered orphan genes and antievolutionists have touted them as evidence against evolution since they appear not to have precursors in other species. Further evaluation revealed this area of the chromosome had undergone extensive genomic rearrangements not present in other apes. The 8 different human only microRNA genes in that area were embedded within an array of ribosomal RNA genes and these microRNA genes resemble parts of the rRNA genes. It appears that as the rRNA genes underwent segmental duplications that a part of them broke off and formed the smaller microRNA genes. This would be the first evidence of de novo new gene formation through genomic rearrangements. (7). Researchers in Finland have also shown how new microRNA genes have arisen out of DNA copying mistakes by looking at their signature palindromes (7a).
Scientists knocked out the flagella regulatory gene fleQ for the proper function of a bacterial flagellum. They then put the bacteria under strong selection to regain mobility. The bacteria used two independent random mutations to regain the lost flagella in 4 days. They did this by diverting a related regulator gene to switch from controlling nitrogen uptake to instead control flagella biosynthesis. The bacteria co-opted a regular gene normally not involved in flagella formation (11).
In terms of gene duplications, it’s hard to beat plants. They often completely duplicate their entire genomes and sometimes several times over. This is called polyploidy. This frees up many parts of their genomes to develop new genes and new functions. Scientists studying the specialized carnivorous Asian pitcher plant, or Nepenthes, found it had a decapod genome in its diploid state, a complex structure almost unprecedented in flower plants that reflected a five whole-genome multiples. One of the subdomains was dominant, but the others were free to evolve new functions. The enzymes that help Nepenthes break down insects’ hard exoskeletons, for example, were repurposed from those that originally shielded plants from being eaten by those animals. (8).
Three new genes were produced by a copy and paste duplication error involving the NOTCH gene, called the NOTCH 2NL group. They created new proteins that in the human fetus helped human brains to enlarge from the original NOTCH gene (10).
In addition, thousands of random segmental duplications that include genes have been identified and noted to be shared often by other species. If we find the same random segmental duplications shared between species this is near proof of common descent. This is discussed in the blog on duplications and evolution.
2. Horizontal or Lateral Gene Transfer
This happens mostly in prokaryotes like bacteria. New genes are acquired by bacteria exchanging DNA, often mediated by viruses called phages that pick up DNA from an infection in one cell before transferring it to another cell after budding off. Mitochondrial DNA (which are cellular organelles that have their own DNA - see blog and how we know mitochondria were former bacteria and can have some of their DNA transferred to the host nuclear DNA through a DNA repair process. See how shared DNA repairs between species proves evolution (2). Since this type of obtaining new genes is not a significant method for multicellular life little more will be discussed.
3. Gene Fusion and Fission
Genes can also fuse or undergo fission thereby forming new genes. “Interestingly, it has been observed that chimeric fusion genes sometimes involve two copies of the same gene (e.g., the alcohol dehydrogenase gene in Drosophila), and when that happens, the resulting genes undergo parallel evolution in which they shift away from the functions of their parental genes.” (2)
4. Transposable Element Protein Domestication
TEs are segments of DNA that have the ability to copy themselves and randomly jump around in the genome. They increase the genome size but usually do not code proteins. A genome can acquire new genes by recruiting transposable element proteins and using them as cellular proteins. It is estimated that about 45% of the human genome is derived from retroviral infections and their viral derivatives (retrotransposons for example). Many TE domesticated proteins have been identified and some play a role in vertebrate immune system and light sensing in plants (2).
In addition, various TEs - “jumping genes” - have been identified in human genomes. We have found the same random jumping genes shared by other species in the same homologous locations. Because they jump randomly, if we find the same TE in the same location between species often with the same mutations the only conclusion is common ancestry; common design as an explanation becomes intellectually impossible. This is discussed further in the bog on how shared TEs prove evolution.
Possible Objection - the anti-evolutionist could claim that these new genes with new applications and “information” still had to come from pre-existing genes that were changed. At a minimum these examples disprove the idea of no new genes and information; they do indeed introduce new genes and new information into the genome. Speciation and phenotypic changes occur not just from disabling existing original genes. What if the new genes from duplications themselves are duplicated and produce further new genes, resulting in a steady or even exponential incremental increase in information and complexity - exactly what we see in the fossil record? Evolutionary compound interest? If this new information and products influence other parts of the genome what inhibits incremental coordinated phenotypic changes to better serve a changing environment? Disabling genes at the same time new genes were being produced would seem to be a method for how evolution could be driven at the molecular level let alone if drift accelerates or influences the entire process.
What many are interested in however are genes that arose de novo. This is something usually anti-evolutionists claim can’t happen. De novo genes would answer the creationist claims that orphan genes (ones that don’t have known other similar genes in evolutionary related species) disprove evolution. Actually they support it by demonstrating why they are unique - they arose de novo. Instead of being a problem for evolution, they support it while explaining where new information comes from to supply raw material for natural selection to change species. Mic drop. This is similar to creationist discussions that certain structures in the vertebrate eye are designed when in truth the four aspects of the vertebrate eye that they think are wonderful eye designs only exist because solutions are needed to patch up the consequences of having an inverted retina that compromises vision. See section 1h in the blog on unintelligent design for a discussion and visual diagrams of the four workarounds provided by natural selection to attenuate the poor design of the vertebrate eye. Those four structures speak to poor design in the vertebrate eye necessitating natural selection work arounds rather than a great “design”. Duct tape over a broken car tail light is not a great original engineering design.
De Novo Gene Formation
A classic story of new gene formation involves Ice Fish antifreeze proteins and will be discussed below in a separate section.
Caroline Weisman published a paper in the Journal of Molecular Evolution in 2022 entitled “The Origins and Functions of De Novo Genes: Against All Odds?” A de novo gene was one that “evolved from previously non-genic DNA”, something thought to be rare as it would be unlikely that random sequence would produce a functional gene. (9)
She listed her criteria for a true de novo gene:
“First, I require positive evidence of the gene’s absence from outgroup species. For RNA genes [non coding genes], there must be evidence that the orthologous sequence is not transcribed, or that it produces a substantially different transcript, in outgroups. For protein-coding genes, there must be evidence that the orthologous sequence is not translated, or that the ORF [open reading frame] is substantially different, in outgroups. Note that the failure of, e.g., BLAST to detect homologs in outgroups, a common methodology, does not constitute such evidence.
Second, I require at least two outgroups for which the above is true. This is the minimum number required to make de novo gene gain likelier than the alternative of gene loss in outgroups, assuming (generously) that these events are equally likely.
Finally, I require data suggesting that the gene has a biological effect, in the form of an observable phenotype when it is knocked out or down. For protein-coding genes, there must be some evidence that this phenotype is due to the novel protein rather than the transcript. (As others have noted, the word “function,” especially for de novo genes, is fraught (Keeling 2019); when I use it here, it is as shorthand for this criterion of “producing a biological effect,” and does not imply other frequently associated concepts like having been evolutionarily selected.)”
Wiseman then goes on to list some of the protein and non-protein (RNA) coding genes that have been identified as true de novo genes according to her strict criteria
1. Saccharomyces cerevisiae MDF1
Originated de novo within the last few million years. Represses expression of genes in the mating pathway.
2. Sacchromyces cerevisiae BSC4
First de novo gene subjected to experimental structural characterization
3. Homo sapiens PBOV1
Found in an intron of the conserved gene BIG3, on the opposite strand. Originated de novo in humans or hominid primates. Over expressed in various cancers.
4. Homo sapiens NYCM
Overlaps the well known oncogene MYCN. Likely emerged either uniquely to humans or prior to the split with chimpanzees. It is arguably the best experimentally characterized of all the de novo genes. Contributes to oncogenesis.
5. Homo sapiens MYEOV
Role in cancers.
6.Homo sapiens ELFN1-AS1
RNA gene unique to humans, in the intron for conserved gene ELFN1
Promotes various cancers by increasing cell proliferation.
7. Mus musculus Poldi
Noncoding RNA in several Mus species likely emerged around 3 million years ago. It is expressed in the post meiotic round spermatids.
She goes on to note: Much of the noncoding DNA is subject to a low rate of reading, called pervasive and promiscuous transcription and translation. Some of these random sequences do actually produce products that have surprisingly similar structural features shared by known proteins. Related work has often found intergenic open reading frames which can provide raw material for de novo genes to arise. A “transmembrane-first” model is the first proposed cell biological mechanism for de novo gene birth. Two genes, MYEOV and MDDF1 act as transcription factors by dimerizing with conserved transcription factors that under different conditions have different binding partners. They then drive expression of the same promoters but under different conditions. (9)
This is considered by some to be a program primarily used in development which is then reactivated in cancer, allowing mature tissues to aberrantly migrate and metastasize. Others of these genes aberrantly activate other pathways used elsewhere in normal physiology, like TGF-B signaling… New proteins may generally find it easy to flip all kinds of cellular switches; cancer may often be the result she notes (9).
Cancer and Evolution
Note that many of the new genes Weisman lists above are associated with cancer. The role evolution plays as a model for cancer can’t be under appreciated. It would be interesting if there are any anti-evolutionists who study cancer at the molecular level.
The word cancer comes from a transliteration of the Greek word for crab in Latin. It is a term used since Hippocrates to denote types of tumors that show abnormal growth in the shape of a crab. Today we also have the words carcinogen and carcinoma. In astrology it is the fourth sign of the Zodiac and it also refers to a constellation. The study of cancer can give us great insights into evolution since cancer begins from a few mutations in a single normal behaving cell and then begins to develop more mutations in a nested series that adds new genes (A, A+B, A+B+C,…) and functions to a mass of cells that goes rogue, growing according to principles of natural selection (some mutated cells are better at surviving and reproducing than others). It leaves a record of the mutations that resemble evolutionary trees in biology and researchers can work backwards to know when in the tumor growth for example a mutation occurred and spread. It is not evolution per se, but rather a model of what happens on a species population level as new genes form and can be selected. A cancer that begins as a cell disobeying its host constraints, must develop new genes and functions to avoid the body’s immune system, often the ability to move to other parts to invade (metastasize), and the ability to outcompete normal cells for nutrients and other cells and tissues. It did not have these functions before mutating them. Yes, random mutations can generate new genes with new functions.
“Evolutionary theory “makes sense” of cancer, giving us critical insight into how it works. This has become particularly clear in recent years. Now, we can sequence all the genes in a patient’s cancer, and see how they change over time as cancer evolves. Cancer evolves with the same evolutionary mechanisms that drive the evolution of new species. Like breadcrumbs marking a path through a forest, cancer evolution leaves information in cellular genomes that evolutionary theory can decode.
Going the other direction, cancer makes sense of evolution too. Cancer itself is not evolution at the species level. However, it validates the mathematical framework underlying modern evolutionary theory. Cancer cells evolve multiple new functions in an evolutionary process, creating precise genetic signatures of common descent. At both a genetic and functional level, cancer follows patterns explained by evolutionary theory…In cancer… we can directly verify that evolutionary theory correctly reconstructs a cancer’s history, including its ancestry. We see all the same patterns in cancer evolution that we do in the evolution of species: neutral drift, nested clades, novel functions, and positive selection. The same math, software, and theory that is used to study the evolution of species works for cancer too.
From a biological point of view, it is now clear that cancer is an evolutionary disease. Cancer biologists use evolutionary theory because it is useful and accurate, not because they are pushing an “evolutionary agenda.” In cancer, cells evolve a set of new functions. These functions are beneficial to the cancer cell, but ultimately lethal to their host. And cancer must do much more than just grow quickly.
Nonetheless, in all cases, more than just rapid growth is required for cancer to develop. Several new functions are required. Ultimately, many cancers will acquire more than ten beneficial (to the cancer cell) mutations that enable these new functions. Evolution, it turns out, is a much more useful framework for understanding cancer. From the cell’s point of view, cancer is evolving new functions in the environment of the host’s body. It evolves these functions in an evolutionary process. Cancer exists only because biological systems, including humans, have the intrinsic ability to evolve.”
~ Joshua Swamidass, MS, MD, PhD. Associate Professor of Laboratory and Genomic Medicine, the Washington University School of Medicine in St. Louis.
From the blog, this site : Evolutionary Medicine. Is it important?
A Tale of Two Fishes*
No discussion of new genes and new functions arising naturally would be complete without talking about the anti-freeze adaptation found in some fishes. And yes, in science when talking about more than one species of fish, it’s fishes.
Notothenoid fishes (Southern Ocean)
It has been known for many years that some fish species in the arctic and antarctic regions survive subfreezing temperatures through the use of anti-freeze like glycoproteins (afgps). These proteins bond with any ice forming in the fishes and stop the crystals from connecting to other ice crystals by lowering the freezing point of body fluids. One of the first groups studied were the predominate group of notothenoid fishes of the antarctic (southern) ocean. In 1997 Chen et. al. worked out the evolution of these afgps.
“We have found that the antifreeze glycoproteins (AFGPs) of the predominant Antarctic fish taxon, the notothenioids, evolved from a pancreatic trypsinogen… The primordial AFGP gene apparently arose through recruitment of the 5′ and 3′ ends of an ancestral trypsinogen gene, which provided the secretory signal and the 3′ untranslated region, respectively, plus de novo amplification of a 9-nt Thr-Ala-Ala coding element from the trypsinogen progenitor to create a new protein coding region for the repetitive tripeptide backbone of the antifreeze protein.” (12).
Note that this is mostly the typical gene duplication method of producing a new product from a previous gene discussed earlier. In this case the original gene was specialized as a pancreatic enzyme. Sequence divergence between the ancestral pancreatic trypsinogen gene and the afgps according to the researchers indicated an origin of the antifreeze gene of around 5 - 14 million years ago. A much more recent 2023 paper by Bista et. al. looking at 24 species of the Notothenioidei fish group allowed them to narrow the radiation of this group to 10.7 million years ago origin. Genomic evaluation of the afgp expansion revealed a very complete reconstruction of the radiation of these fish species by comparing the antifreeze glycoprotein gene families (13). This period corresponds to paleoclimatic changes appearing at that time. Global cooling and polar icecap formation was occurring due to the separation of the Antarctic continent from surrounding land masses and the subsequent establishment of the Antarctic Circumpolar Current (ACC) (13). Note that this is another way evolutionary theory reconstructs the past well, combining plate tectonics, continental drift, paleoclimatic changes, and species radiation through the understanding in this case by using comparative genomics of antifreeze proteins in a group of fishes!
Codfishes (Arctic Ocean)
In studying the Atlantic codfish’s evolved antifreeze protein researchers were surprised to find that instead of its origin being in gene duplications from existing genes as in the notothenioids, “this protein had seemingly been built from scratch, from desolate stretches of the genome that do not code for functional molecules.” This species, Gadus morhua, had an antifreeze protein that was produced from a de novo gene. (15).
Baalsrud et. al. determined that the afp in Codfish was de novo and not from duplications by several findings (14):
First, they performed a BLAST and did not get any hits against any part of the afgp in genes or ORFs (open reading frame) in high quality codfish genomes. Neither did they get hits in Uniport, the Ensembl genomes, or Genbank. The gene is an orphan gene.
Secondly, de novo genes are more likely to arise in GC-rich genomic regions as these regions are more active in transcription and more likely to obtain an ORF because of stop codons that are AT-rich. GC content in the afgp copies was as high as 76% vs. 56% on average for all genes in the G. morhua genome assembly.
Third, they calculated codon usage and there was a significant bias for the amino acids in the repeats across all the afgps in the codfish species being investigated. “This finding, together with the afgps on a single linkage group with well conserved synteny between the G. morgue and M. aegllefinus strongly suggests common origin of codfish afgps, with subsequent gene duplications.”
Fourth, a protein translated from non-coding DNA is intrinsically more disordered. They used a program to determine intrinsic structure disorder (ISD) for all four functional afgps in G. morhua. The values for disorder (.68 and .75) were much higher than the average mean ISD for all the annotated genes in the G. morhua genome of .36.
Summary: Antifreeze fishes
Research has shown that the antifreeze proteins found in the antarctic fish Notothenioidei evolved mostly by gene duplications, although even in this gene there is a de novo amplification of a 9-nt Thr-Ala-Ala coding element from the trypsinogen progenitor. Conversely, in the northern arctic areas codfish antifreeze proteins evolved by de novo gene formation followed by gene duplications. The evolution of these proteins allowed various species of fish in sea regions that were now experiencing freezing temperatures to remain as continental movements and changing paleoclimate forced other tropical species to move out, leaving open niches for the remaining fish species to fill who could succeed in a harsh environment. The evolution of afps coincided with paleoclimatic changes that produced ice and glaciers near the poles millions of years ago.
In the past 10 years researchers have found numerous newly minted de novo genes including in fruit flies, mice, humans and important crop plants so de novo gene evolution may not be as rare as researchers thought in the past. (15). “De novo gene origin has recently become more widely recognized as a regular source of new genes (Tautz and Domazet-Lošo 2011; Wu et al. 2011; McLysaght and Guerzoni 2015; Schlötterer 2015; McLysaght and Hurst 2016), which often encode novel functions representing lineage specific adaptations to the environment (Khalturin et al. 2009; Tautz and Domazet-Lošo 2011)." (14)
*Note - the evolution of antifreeze proteins has actually occurred in many species, and not just fish. “… the evolution of the antifreeze proteins (AFPs), which have evolved independently in bacteria, plants (≥ four times), fungi, insects (≥ two times), and teleost fish (≥ seven times) (Cheng 1998; Ewart et al. 1999; Harding et al. 2003; Bildanova et al. 2013; Gupta and Deswal 2014) (14). Many of you may have noticed that anti-freeze proteins are a fantastic example of convergent evolution across many varied species. My apologies to Charles Dickens for attempting to have some increased credibility bestowed upon this humble author by indirectly, and hopefully not inappropriately, associating the story of ice fish evolution with a famous book.
Proto-Genes
Ideally, if genes were forming de novo it would be nice to see early steps and transitions: pre-genic DNA coming together in the forms of proto-genes. This has been noted in the E. coli Long-Term Evolution Experiment (LTEE). Researchers noted how proto-genes originated by starting in one of two acquisitions. They wrote,
"... we identified instances of proto-gene emergence in which a previously unexpressed sequence was transcribed after formation of an upstream promoter. Tracing the origin of the causative mutations, we discovered that most occurred early in the history of the LTEE, often within the first 20,000 generations, and became fixed soon after emergence. Our findings show that proto-genes emerge frequently and within evolving populations, persist stably, and can serve as potential substrates for new gene formation." (16)
This is shown graphically below:
From: Genes From The Junkyard. Adam Levy. Nature, vol 574, Oct. 17, 2019. Fair use attribution. For educational purposes only. (15)
Conclusion
Even the most fundamentalist anti-evolutionist who believes the entire human population at one time along with all the terrestrial animals were wiped out and then rebooted from only a few pairs of “kinds" on a boat a few thousands of years ago understands that natural selection is intuitive. Various pressures on populations of animals and plants will result in the most fit for survival and reproduction leaving more offspring to the next generation on average and populations will thus evolve to fit the present circumstances of that species. If shifts occur in the environment for example, the species can adapt. Unless those shifts are too sudden and strong (asteroids), or the species does not have the variations needed, or perhaps the species became too specialized and runs out of options, the species can evolve to meet the changes. This has been called “microevolution” and no one rejects this who understands it. Evolution has been defined since at least the 1940s as the change in gene frequencies or alleles in a population over time. See Evolution, this site. We see that every day in the lab, field and in medicine. Even those few “kinds” coming off a boat at one time had to evolve into the millions of flora and faunal species we see today in only a few hundred years (never mind that this is impossible rationally).
What about large scale changes like we see in the fossil record, a nearly 15,000 ft collection of sedimentary rock showing changes from simple to complex as in layers of a massive tall cake with no mixing and lots of transitional fossils? That faunal succession would need new information, new genes to produce very different phenotypes, structures, and biochemical pathways. If “macroevolution” is true then where did the new genes come from to make those new adaptations?
Scientists have identified five major methods for new genes to arise: duplications and then new functions off the copied genes, lateral gene transfer from outside the organism, gene fusions and fissions, co-option of transposons, and with some surprise, de novo genes. The last category is important because it negates the criticism that is often brought forward by creationists and anti-evolutionists that the others only operate from pre-existing genes. This article has shown that nature can and does generate functional genes from non-gene, non-coding raw DNA material. It is thus a false statement to say new genes, new information for various selection forces can’t arise through natural means only. This final objection to evolution attempting to negate variation sources for natural selection and other mechanisms to push “macroevolution” changes can be dismissed. Together with the newer DNA findings that rise to the level of proof of human evolution and macroevolution, there are no intellectually honest viable objections to evolution remaining. Random mutational activity is demonstrated to produce the raw material for evolution. Random changes to our genomes that are shared by other species rises to the level of proof that macroevolution, human evolution is a fact. See The Demise of Evolution Objections. The theory of Evolution, that which explains the origin of species, has passed every challenge and test to it for 150 years and grows stronger with passing time. For human interests, how we got here, when, from what and from where goes a long way to explaining the “why’s” of life and its many existential questions. Notwithstanding, discovering perhaps the most amazing true, and fascinating story ever revealed has value in its own right.
Literature cited
1. Behe, Michael J. 2019. Darwin Devolves. HarperCollins, New York, NY 10007. Paperback, 2020. 342 pp.
2. On the Origin of New Genes and Pseudogenes.
3. Finlay, Graeme. 2021 (paperback). Human Evolution: Genes, Genealogies and Phylogenies. Cambridge University Press. University Printing House, UK. 359 pp.
4. Venom evolution through gene duplications.
5. Gene Genesis: Scientists Observe New Genes Evolving From Mutated Copies.
6. Real-Time Evolution of New Genes by Innovation, Amplification, and Divergence.
7. Witnessing the Birth of human-specific genes
https://onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.24504 7a. New genes found that can arise "from nothing" https://phys.org/news/2023-12-genes.html?fbclid=IwAR3auKKirGzwBN0VHc4xC1-ZZQPs2XR_wNoELyAvS4tiX6nTOkDhucS12X4https://phys.org/news/2023-12-genes.html?fbclid=IwAR3auKKirGzwBN0VHc4xC1-ZZQPs2XR_wNoELyAvS4tiX6nTOkDhucS12X4
8. Genomic study sheds light on how carnivorous Asian pitcher plants acquired signature insect trap.
9. The Origins and Functions of De Novo Genes: Against All Odds?
10. Genetic error led humans to evolve bigger more vulnerable brains
11. Two step mutations to rewire a regulatory network via natural selection
12. Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish.
13. Genomics of cold adaptations in the Antarctic notothenioid fish radiation.
14. De Novo Gene Evolution of Antifreeze Glycoproteins in Codfishes Revealed by Whole Genome Sequence Data.
15. Genes From the Junkyard. Levy, Adam
16. Promoter capture drives the emergence of proto-genes in Escherichia coli https://www.biorxiv.org/content/10.1101/2023.11.15.567300v1.full
17. The End of Evolution? A biochemist's crusade to overturn evolution misrepresents theory and ignores evidence. https://www.science.org/doi/10.1126/science.aaw4056
