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  • Writer's pictureJon Peters

Jumping Genes: Macroevolution Validation

Updated: Dec 20, 2023

“It is generally stated that half of our genome is derived from ERVs and TEs. The application of more-sophisticated software allows the identification of more degenerated (fragmented) TEs has raised this estimate to two-thirds of our genome. TEs have expanded, modified, and elaborated our ancestors’ genomes at least as far back as genetic analysis can detect.” ~ Graeme Finlay,

Human Evolution: Genes, Genealogies, and Phylogenies. 2013.


The year 1953 was an incredible year for biology. A paper by Watson and Crick was published that finally ended the search for the source of heredity and cell functioning for all living things. Proteins, the early candidate, had been toppled by DNA. No one could imagine initially that a molecule with only four nucleotide bases - A,T,C,G - could be the holder of the instructions for life. Shown without her knowledge, Rosalind Franklin’s photograph of DNA helped Francis and Crick put one of the final pieces of the puzzle in place. Watson, Crick and Wilkins later received the Nobel Prize in Physiology or Medicine in 1962 for the discovery that DNA encoded the genetic information for life.

DNA was thought by many to be like a blueprint, locked away safely in the nucleus. Messenger RNA (mRNA) would make a copy of one side of the unzipped double helix master code and then the mRNA would travel outside of the nucleus to the ribosome factories to help assemble proteins. Perhaps you also have thought of DNA as a master blueprint.

Decades later as scientists studied DNA more closely one of those scientists, Barbara McClintock, shocked the world when she demonstrated that large amounts of DNA jumped around randomly copying and pasting back into the DNA, often causing disabled genes. Genomes were not this rigid instruction blueprint as imagined. Indeed, the corn she was studying was made up a whopping 90% of these mobile DNA segments. Humans were found to have nearly 50% of our 3 billion DNA nucleotides made up these mobile elements alone, called transposable elements or TEs. (1)

Transposable Elements (TEs)

There are over 1,000 different types of TEs, or jumping genes, and about 50% of our genome is made of them but there are only two basic categories of TEs. DNA transposons and ones that use RNA as an intermediate, and are called retrotransposons. No, the retro does not refer to 1960’s bright plastic furniture or 1970’s colors of gold and green. This latter variety must convert their RNA to DNA so it can be randomly spliced into the DNA genome rather than the normal route of DNA to RNA to proteins. The DNA transposons only represent about 2% of our genome and won’t be discussed since they are not necessary to establish evolution (2).

The more common retrotransposon TEs are represented by several types important to our discussion. One type makes up 8% of our genome and includes the endogenous retroviruses (ERVs) that were discussed in a section on this site. They are fantastic evidence for evolution and common ancestry by themselves. ERVs have 3 major viral genes (gag, pol, env) for producing their nasty retroviral cellular parasites; an example is the retrovirus HIV that can produce AIDS. Some have lost the env gene and are called LTR-retrotransposons. As was discussed in the section on ERVs, ERVs are fossilized by mutations and the retroviruses are no longer able to produce infectious particles. Most are so degraded only their LTRs are left behind. But initially they were inserted randomly by retroviruses, and if we find thousands of the same ERVs in the same locations between species the only rational conclusion is shared ancestry - evolution. They must have inserted before the species split. The LTRs are made by the viruses before insertion since they will need promoters to get transcription started to make new viral progeny during an infection.

Most retrotransposon varieties however do not have an LTR attached and are non-LTR retroelements. Two are especially important for our purposes here. LINEs are long elements of about 6,000 base pairs and SINEs are short and only about 300 bases long. The most common SINE are called Alu elements, named after the bacteria Arthrobacter luteus where their enzyme product was studied. LINE-1 elements alone make up a staggering 17% of the human genome (626,000) and Alus another 11% (1.1 million). There are also L-1 and L-2 retroposons in our genome for another 340,000 (2). Thus LINE-1s, Alus, and LTR retrotransposons alone make up 36% of the human genome! Considering humans have only 25,000 genes and 20,000 protein coding genes make up only 1.5% of our genome, the 50% of our genome that are retrotransposons is amazing. Much of the TE’s are selfish jumping DNA that cause disease when they land and disable genes or adversely affect them. But nature through shared interspecies TEs has supplied us with rock solid evidence for evolution because when they move they insert randomly and since we find thousands of them in identical homologous locations (called loci) in the genomes of different species, we have evidence for evolution that rises to the level of proof. Indeed, “macroevolution” level proof. These shared TEs must have inserted before then species split. And yes technically science rarely if ever proves - but evidence can be amassed to such a level that to deny a conclusion is perverse. Fortunately, most have lost the ability to move but for millions of years many did, leaving a record that can only be rationally explained by evolution.

1. LINE-1 Elements

As with other retrotransposons when LINE elements land in genes they often disrupt them. A LINE-1 that is found in an exon (active part) of a gene called the APC gene, a tumor suppressor gene, together with other mutations inactivated the gene; it is not working in 80% of all human colon cancers. A canine tumor (CTVT) has a LINE-1 element inserted near an important proto-oncogene. LINE-1s insert like ERVs insert (2).

Recall that retroelements copy and then randomly paste themselves back into the DNA. Of the approximately 600,000 LINE-1 elements in the human genome all but 2,000 are shared exactly with chimps and bonobos. As with ERVs, this means that over 99% of the LINE-1s in our genome have exact matches by location and ATCG sequences with chimps. Our genomes share all LINE-1 elements with gorillas except for 1,860. Some LINE-1 elements on rare occasions will grab a random RNA segment and then make a two-component element with the usual LINE-1 portion and an ‘innocent bystander RNA” (2). This results in a very unique LINE-1, a chimeric retrotransposon that have been found in human genomes and are especially solid evidence for evolution since they produce very unique shared markers also present between species; a common ancestor is the only rational conclusion.

Not only can we find thousands of the same retrotransposons in the same genomic positions between species establishing evolution because they insert randomly and must have done so before the species split, but some are shared by some species and some not. If we collect hundreds and note which are shared between and which are not a pattern is produced that shows evolution in remarkable detail. Using molecular clock calculations we can also determine when the species split and compare those results to the paleontology (fossil) data. The data cries out evolution because there is so much of it across so many independent areas of science. In the case of DNA findings it rises to the level of proof of even macroevolution. Notice that this evidence for evolution is independent from function or not. More will be said about function. See Figure 1 below:

Figure 1. Various LINE-1 insertions entered into the Primate Germ line, from their presence or absence in the genomes of primate species.

LINE-1 elements: Open boxes. Chimeric inserts = grey boxes. Numbers indicate the number of individual inserts mapped. See text for discussion. From: Finlay, Graeme. 2021. Human Evolution: Genes, Genealogies and Phylogenies.

p 85. Figure 2.5. Cambridge University Press. Social sharing and Fair dealing applied per publisher's web instructions. Paperback edition.

2. Alu Elements

The origin of most retroelements have been lost in deep time. We do know however how Alus arose. Millions of years ago a gene called 7SL gene, important in signal recognition, fused to form a double DNA piece (called A and B sides) with a short section of an A-rich region between. It has an internal RNA promoter. Each Alu is unique in terms of accumulated mutations, the length, and the 3’ end. (3). Alus are only found in primates so we can determine evolutionarily about when primate evolution occurred.

Of the 1.1 million Alus in the human genome, all but 7,000 are shared by chimps and bonobos. That again is greater than 99% shared Alus. Only a few thousand Alus in the human genome are not found in gorillas, establishing that Alus demonstrate the African great ape ancestor also had 99% of the Alu elements that humans, chimps and gorillas have. The only rational explanation is that these Alus must have copied and pasted back into the DNA in a common ancestor to the great apes. As in LINE-1s, some are shared by all primates and some by only some. By just collecting these raw observations one can produce an evolutionary phylogenetic tree demonstrating primate evolution, which most people would describe as “macroevolution” since it involves so many primate species, from macaques to humans. Out of the 1.1 million Alus found in humans, all are shared by orangutans except for 250, establishing a common ancestor between humans and orangutans. (2).

Figure 2 shows an Alu insert into the HPRT gene found in multiple species including humans, chimps and gorillas but not other primates establishing evolutionary relationships. Notice the target site of [GAATGTTGTGA] where the insert happened and how the target site was duplicated and placed on either side of the changed DNA, confirming the insertion. Inactivation of this gene produces Lesch-Nyhan syndrome, a condition in children that produces gout, mental retardation, and self mutilation (2).

Figure 2. The insertion of an Alu element in the HPRT gene.

From: Finlay, Graeme. 2021. Human Evolution: Genes, Genealogies and Phylogenies.

p 90. Figure 2.7. Cambridge University Press. Social sharing and Fair dealing applied per publisher's web instructions. Paperback edition. See text for discussion.

Below in Figure 3 is the distribution of many Alu elements in various primate genomes. By simply noting which are shared by what groups an evolutionary phylogenetic tree is produced. This transposon evidence for evolution not only agrees with thousands of other DNA trees produced by shared ERVs, shared duplications, shared DNA breaks/repairs, and shared pseudogenes but also agrees with evolutionary trees produced by fossil observations (paleontology).

Figure 3. Distribution of various Alu elements in primate genomes.

Check marks and circles indicate presence and absence of particular inserts. Shading corresponds to the shading of the boxes and arrows, indicating when the Alu elements were added to the primate germ line. From: Finlay, Graeme. 2021. Human Evolution: Genes, Genealogies and Phylogenies.

p 91. Figure 2.9. Cambridge University Press. Social sharing and Fair dealing applied per publisher's web instructions. Paperback edition.

Are the insertions really random?

Yes, they are. Turns out that LINE-1s and Alus do have some site preferences, but still not exact site insertion locations, or loci (4). Looking at any figures such as Figure 2, we can see that when they insert into a target site in the DNA, that area is duplicated on either side of the target, called Target Site Duplications (TSDs). Thus, we can find LINE-1s and Alus not only by their signatures but also by these TSDs. They are not original to the DNA. The idea that millions of TEs would randomly insert in the same exact genomic locations between species is mathematically impossible.

What about hot spots?

TEs do have preferences for insertions. They tend to insert around genes and also some prefer to insert into existing TEs. But these are preferences and not exclusive to the exact loci. As an analogy, there are car accident hot spots in cities where car accidents are more prone, but they are still accidents and each one is unique. Some cities have large numbers of people moving to them but they don’t all move onto the same street and certainly not into the same house.

In neurofibromatosis type 1 the NF1 gene is mutated. “…of all the NF1 mutations, 0.4% are caused by retrotransposon insertions. In one study, 18 TE insertion mutations were identified in unrelated people, and six of these were clustered in a region of 1,500 bases. Three insertion sites were used twice…of the three sites that were targeted twice, all could be shown to be independent events… the TSDs were of different lengths, the initial cleavage events were on opposite strands of the DNA, or Alu elements of different sub-families were involved.”(2).

In one study, 500 LINE-1 elements associated with the human genome were studied. In any other species did any LINE-1 element insert into any of those 500 sites? Not a single one. (2). Studies with Alu elements have also shown the same result. Human specific Alus were studied and “in no case was an Alu element characteristic of sub-families belonging to other species found in the same site as the human insert… It has been concluded that ‘no instances of insertion homoplasy in hominids have been recovered from the analysis of >2,500 recently inserted human Alu insertions’ (2).

Exceptions: Incomplete Linkage Sorting

It turns out that when comparing genomes there are many exceptions to the clustering of inserts into evolutionary phylogenetic trees. As an example, TEs have been found to be inserted into gorillas and humans but not chimps. Doesn’t this invalidate using TEs or other DNA changes as markers for evolution? Not at all.

What is going on is called incomplete linkage sorting (ILS). Our genomes are made up of many different alleles, which are possible genes at a given location or locus. As an example, with the major blood group ABO, one can be OO, AO, BO, AB, AA or BB. Because we normally get one chromosome from each parent there are only two possible places for these specific multiple alleles. With the immune system for example there is an MHC complex where hundreds of possible alleles for a gene are available. Genes that have multiple possible alleles are called polymorphic. If speciation occurs rapidly relative to the time required for it to become fixed in a population (where all members have it), a new species may randomly lose a particular gene by chance and genetic drift when it splits off from the ancestor species.

Anti-evolutionists made a big deal in 2012 after the gorilla genome was sequenced and it was found that up to 30% of the chimp, human and gorilla genomes showed incomplete linkage sorting (5). Considering that a particular critic of evolution is perhaps the leading creationist geneticist the attempt at obscuration and misrepresenting the findings was breathtaking. We’ve met Dr. Tomkins before in several other blogs on this site. See human chromosome 2 fusion , pseudogenes, and especially by Dr. Zach Hancock. Dr. Tomkins is arguably the most prolific Young Earth Creationist writer in terms of genetics. It seems lost on anti-evolutionists that ILS is expected, noted and actually was predicted from population genetics by Kingman in 1982 (6). Instead of bad news for evolution this apparent anomaly in phylogenetic analysis actually supports evolution due to calculations, and the real apparent problem is why a top creationist apologist in genetics seems to have left his PhD back at his granting institution. For an explanation of ISL - it’s not easy to understand - see an article at The Panda’s Thumb and Freethought Blogs (7). One of the best insights possible into erroneous anti-evolution claims is drilling down on their arguments to expose fallacies, often committed by omission.

Macroevolution deeper in time

You may have noticed that the few examples I’ve extracted from Finlay’s book are primate centered. Perhaps you are wondering if these jumping TEs can be traced further back in time to show evolution earlier with even more distant shared common ancestors, like those evolutionary trees that scientists have produced through anatomy and fossils - a tree of life or more accurately a bush of life? And the answer is yes. Of course after millions of years TEs have become so degraded that there are limits.

After the mouse genome was sequenced it was compared to our genome and studies showed there were large numbers of shared TEs. In particular LTR, LINE-1, LINE-2 and MIR (mammalian repeat) elements. “In a DNA segment encompassing 1 million DNA bases from the two species, 13 LINE-2 and 30 MIR elements were shown to be shared…inherited from the ancestor in which each element entered the DNA” (2). Finlay notes:

“Computational searches have identified five TEs that are shared by primates and tree shrews, and in one case, by the flying lemur. These are all absent from rodents. On the one hand nine TEs were found to be shared by rodents and rabbits but are absent from primates. Primates, tree shrews, and flying lemurs form one monophyletic group; rodents, rabbits comprise another. But ultimately, we and the mice in the garden share many TEs each which arose in the genome of a Euarchontoglires [a clade and superorder of mammals that groups rodents, rabbits, primates and a few others based on TEs] ancestor” (2, pg. 105).

Multi-species genomic comparisons have found several well-preserved TEs that corroborate shared ancestry in many species. One is an insertion site of a L1MB3 element. Humans share this TE with cows, horses, cats, dogs, bats and shrews. The degenerated undisturbed target site TACCTGGGAAACTTT is duplicated from the insertion on either side of the L1MB3 transposon (2).

“As an illustrative example, an ancient MIR element in an intron of the beta-fibrinogen gene as been identified in the genomes of 22 species (Figure 4 below). The target site where the DNA was cut has the five base TTACT sequence. That sequence is retained in one of the target-site duplications of 8 species… and can be obtained by a one-base change in 18 other cases. We share this ancient TE with elephants” (2).

Figure 4. Insertion of a MIR element in intron 7 of the beta-fibrinogen gene of various species demonstrating shared ancestry well beyond primate common ancestry. E - Euarchontoglires. L - Laurasiatheria. A - Afrotheria. From: Finlay, Graeme. 2021. Human Evolution: Genes, Genealogies and Phylogenies.

p 107. Figure 2.15. Cambridge University Press. Social sharing and Fair dealing applied per publisher's web instructions. Paperback edition.

A set of TEs was found to be shared by whales and hippos demonstrating that whales and hippos shared a common ancestor. Scientists moved whales into the order containing hippos, pigs, deer, sheep, cattle and giraffes based on this finding. Fossil whales were also found to have a special bone in their ankle confirming their artiodactyla ancestry. See my video on whale fossil evidence for evolution. A retrotransposon insertion in baleen whales led to the loss of enamel-capped teeth. See also a short video on DNA evidence for whale evolution. TEs show all living birds are monophyletic (2).

Using shared TEs between genomes one can demonstrate evolution and clustering of species. We share common ancestors by shared TEs with elephants, sloths, armadillos and even birds and reptiles. We do live during a second Galileo moment for theology. Evolution, macroevolution, is true just as Darwin worked out 150+ years ago. The DNA evidence is sound, robust, and will withstand the best anti-evolutionists can bring to bear.

TEs can be beneficial and functional

Until this point the impression has been that TEs jumping around randomly damage a lot of genes and cause disease. They do, but they also have had many positive effects on genomes. Over long ages primate genomes have been invaded by millions of segments of LTRs, LINE-1s, Alus, and SVA elements. Mammals share genomic records of ancient invasions by LINE-2, LINE-3 and MIR retroelements (2).

As Finlay points out TEs have provided DNA sequences for new genes. It is incorrect that evolution has not produced new genes and novel genetic information. By jumping in genomes they have also added to the variety of genes when they land into exons (the parts of genes that are left after splicing out the introns during processing the final gene mRNA). Lastly they have donated segments of DNA that have been co-opted by the host into regulatory networks (2).

New gene examples include the BCYRN1 gene that is functional in nerve tissue. It was formed when an Alu was spliced into the genome of an ancestor to apes and monkeys. Another Alu element produced a family of genes eventually through a series of mutations to form an ASR element then into a CAS element and finally after two duplications into snaR genes. These are transcribed into small RNA regulatory molecules that probably regulate protein synthesis (2). The PMCHL1 and PMCHL2 genes were assembled from genetic parts, one of which was an Alu element. Besides the Alu element, the genes include several downstream exons and a gene duplication. These genes are active in the testes, fetal brain and encode non-coding RNA transcripts (2). Several Alu elements were used to form the FLJ33706 gene that was spliced into the primate germ-line line and later provided a protein-coding sequence (2).

TEs also have provided DNA material for new exons. As mentioned, when the DNA is read to make a final mRNA product that will go to the ribosomes to make proteins, it must first be processed. Most of the transcription is DNA that is nearly always thrown away as introns, leaving only the exons to be spliced together. In the human genome TEs have contributed repeatedly as novel exons. TEs occur in 4.4% of all transcripts and in 0.5% of all DNA sequences that code for proteins. A survey of 330 Alu-derived exons has shown that most are minor components of gene output (2).

TEs have also assumed many regulatory roles. An analysis of eutherian genomes showed at least 16% of all the studied conserved non-coding elements were shown to be formed either wholly or in part by TEs representing multiple families including ERVs, LINE elements, MIR elements and DNA transposons. Non-coding genes produce RNA products for regulation instead of protein products. It appears that 6% of all TEs have acquired stable functions as shown by the fact that they contain sequence motifs that resist change.” (2). Many transcripts in human tissues are initiated from specific sites within TEs and include some fibroblasts, liver, brain and 16% of embryos.

As discussed extensively in another blog about ERVs at this web site regarding retroviruses and the fossilized ERVs they produced, the LTRs present in ERVs have been repeatedly co-oped to be used by the host as promoters for DNA transcription. About 90% of the ERVs in our genome consist only of LTRs, which are functional and 8% of our genome are made of ERVs. About 10% of ERVs have all three genes that hark back to their parasitic infectious origin.

Importantly, most jumping genes either land in areas that cause no damage or have caused few problems. Sometimes two TEs of the same class can join, deleting the DNA between them producing a single chimeric TE (2).

"On short timescales, recombination events, leading to the loss of intervening sequences, cause genetic damage. But on evolutionary timescales, the same processes reorganize genome content, contributing to the transformation of the genome of progenitor species into those of descendent species.” After humans split off from our shared chimp ancestor, more than 70 recombination events occurred between LINE-1 elements resulting in the loss of 450,000 bases… and more than 490 recombination events occurred between Alu elements also and these excised another 400,000 bases from the human genome.”(2).

One gene, SIGLEC13, is present in chimps and Old World Monkeys, accompanied by several Alu elements, but the gene is absent in humans. During our evolution “the entire gene was neatly excised by a recombination event between the left-handmost Alu element and the Alu element just to the right of the last exon.” (2).

Our genome contains many repeated units. If the basic repeat unit is very short, such as only three bases as in -AAG-, the repeat is called a microsatellite. Repeated sequences are often found within LINE-1s and Alu elements. “Microsatellites tend to have high mutation rates… They underlie some 40 genetic diseases…The ability of TEs to introduce such sequences into genomes destabilizes them”. Myotonic dystrophy type 2 developed from an Alu element that appeared in our ancestor and stimulated many repeats perturbing gene function and leading to a genetic disease (2). Host genetic systems do have ways to suppress jumping through epigenetic tags like methyl or acetyl groups.

“Organisms possess regulatory mechanisms to suppress the insertional mutagenesis associated with TE activity. However, such genomic stability may be incompatible with adaptive change over the long term. A high mutational burden is disadvantageous to individuals, but promotes variation upon which natural selection can work, and hence promotes the development of adaptations… Patterns of long-term stability interspersed by bursts of active speciation [by waves of Alu insertions into primate genomes] are well recognized and have been called punctuated equilibrium “ (2, pg. 129).


This discussion of transposable elements (TEs) has been more technical and longer than wished for. Sometimes when it comes to science, brevity is sacrificed for accuracy. Three major types of retrotransposon TEs were discussed: ERVs, LINE-1s, and Alu elements. These three types are examples of non-DNA jumping genes and together constitute 36% of our genome alone. They are called TEs because they can or have in the past jumped around randomly in genomes. Although they have insertional preferences, they insert randomly by specific location (locus). TEs that are shared exactly between species constitute spectacular evidence for evolution, specifically macroevolution. Shared ERVs were discussed in a separate composition about how they are derived from random viral insertions and essentially rise to the level of proof of common ancestry. Why anti-evolution objections fail is also addressed. The two LTRs at the ends of the provirus have in most cases swung around in the distant past during recombination events producing solo LTRs. Most ERVs are only LTRs now and make up an astounding 8% of our genome. Shared LINE-1s and Alu elements between species were discussed in this entry as amazing evidence for evolution also because they also insert randomly and produce nested trees of linked ancestry.

Three important take-aways need to be emphasized. First, TEs insert randomly and we find over 50% of our genome is TE derived. So many unique TEs are shared by other species in the exact same locations often with the same mutations, that the only rational conclusion is species that share the same TEs must have shared a common ancestor in the past. Shared TEs indicate insertions before the compared species split. Like the same scratches on two different rifle bullets must have come from the same rifle (origin) and are admissible in a court of law, so also shared TE’s constitute proof of a shared biological origin since they insert randomly. So much for genomes being like blue-prints and unchanging!

Secondly, the millions of TEs can be nested in evolutionary phylogenetic trees. Some are shared by species being compared and some are not. If we combine them into groups, nested phylogenetic trees are produced and multiple independent trees all rationally point to only one conclusion: macroevolution even going deep in time is a fact. This disproves attempts to explain TEs as a result of a “Fall” since any disease or breaks in the DNA introduced at a proposed "Fall" would not produce nested evolutionary trees.

Third, this jumping is independent of function. Many TEs are functional but the vast majority are not. Most of the time the jumps and new inserts are neutral or cause damage and disease through disabling genes. Over millions of years the host has evolved means to suppress them (methylation and acetylation, e.g.). "Sometimes they jump into very important spots, either genes themselves or in areas of the genome that is important for regulating genes... Joshua-Tor and Ipsaro examined a mouse protein called Asterix/Gtsf1 that immobilizes LTRs" (8). The host as also co-opted many for the host’s own use (especially LTRs which act as promoters and enhancers). To repeat, if TEs were mostly functional or none were, functionality would not matter. It’s the random inserts and the fact that they share the same TEs at the same locations between species that establishes evolution and common ancestry. The topic of functionality is not applicable to the observation of them being randomly inserted and shared between species. This sharing of TEs, producing hundreds of independent phylogenic trees that reach into the deep past, is what also proves macroevolution. A theological and historical appeal to a “Fall” becomes what it always was - a mythological solution to natural observations that only appears on the surface to be explanatory. It was destined to be displaced by science and exposed as fantasy; a literal belief unfortunately that persists and is accepted by billions of people on our planet still.

This is the fifth and final article on this site based on a simple principle - the observation that shared random DNA changes between species can only be rationally explained by evolution and common ancestry. It is suggested if possible that readers just read Finlay’s book that these articles are based on. Only a few examples from his book can be showcased in these articles. The previous four associated articles are ERVs, DNA repairs/patches, segmental duplications and pseudogenes. A proper examination of how we actually observe DNA in compared genomes cries out evolution, and even “macroevolution”. People need only look inward to their bodies for definitive evidence for evolution in themselves. It was there all the time.

To help emphasize the simple principle of shared random DNA markers between species and how they can only be explained by evolution, an organizing post with links to all DNA five articles was produced. In order to counter anti-evolution false objections many of the articles contain answers to common proposed objections. That made the articles longer to be more complete. Even those who accept evolution may not know how strong the evidence from DNA is for “macroevolution” and are encouraged to consider reading those contra-apologetic sections. Some may have realized that all this jumping within genomes would also produce junk DNA. That is a controversial topic unfortunately in biology with even non-religious scientists thinking we have little to no junk DNA. On the contrary, here is an entry arguing junk DNA ? for the opposite situation and based on sound genomic principles.

References and Citations

1. Transposons: The Jumping Genes

2. Finlay, Graeme. 2021. Human Evolution: Genes, Genealogies and Phylogenies. Cambridge University Press. 359 pp. Paperback edition. ISBN 978-1-009-00525-8.

3. Alu elements: know the SINEs

4. Levin, H.L. and Moran, J.V. 2011. Dynamic interactions between transposable elements and their hosts. Nature Reviews Genetics 12: 615-27.

5. Gorilla Genome Is Bad News for Evolution

6. Understanding Incomplete Linkage Sorting.

7. A Tiny Bit of Knowledge is a Dangerous Thing

8. How to Tame a Restless Genome (protein shuts down LTR-transposons)

I think he's wearing blue genes while he jumps........

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