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Theory of Intelligent Design, the best explanation of Origins » Molecular biology of the cell » Genetics » Transposons and Retrotransposons

Transposons and Retrotransposons

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1 Transposons and Retrotransposons on Fri Dec 16, 2016 4:46 pm


Transposons and Retrotransposons

Class I TEs are copied in two stages: first, they are transcribed from DNA to RNA, and the RNA produced is then reverse transcribed to DNA. This copied DNA is then inserted back into the genome at a new position. The reverse transcription step is catalyzed by a reverse transcriptase, which is often encoded by the TE itself. The characteristics of retrotransposons are similar to retroviruses, such as HIV.
Retrotransposons are commonly grouped into three main orders:

  • TEs with long terminal repeats (LTRs), which encode reverse transcriptase, similar to retroviruses

  • Long interspersed nuclear elements (LINEs, LINE-1s, or L1s), which encode reverse transcriptase but lack LTRs, and are transcribed by RNA polymerase II

  • Short interspersed nuclear elements do not encode reverse transcriptase and are transcribed by RNA polymerase III

Class II (DNA transposons)

The cut-and-paste transposition mechanism of class II TEs does not involve an RNA intermediate. The transpositions are catalyzed by several transposase enzymes. Some transposases non-specifically bind to any target site in DNA, whereas others bind to specific target sequences. The transposase makes a staggered cut at the target site resulting in single-strand 5' or 3' DNA overhangs, so-called "sticky ends". This step cuts out the DNA transposon, which is then ligated into a new target site; the process involves activity of a DNA polymerase that fills in gaps and of a DNA ligase that closes the sugar-phosphate backbone.[citation needed] This results in duplication of the target site. The insertion sites of DNA transposons may be identified by short direct repeats (created by the staggered cut in the target DNA and filling in by DNA polymerase) followed by a series of inverted repeats important for the TE excision by transposase. Cut-and-paste TEs may be duplicated if their transposition takes place during S phase of the cell cycle, when a donor site has already been replicated but a target site has not yet been replicated.[citation needed] Such duplications at the target site can result in gene duplication, which plays an important role in genomic evolution.[14]:284 Not all DNA transposons transpose through the cut-and-paste mechanism. In some cases, a replicative transposition is observed in which a transposon replicates itself to a new target site (e.g. helitron (biology)).
Class II TEs comprise less than 2% of the human genome, making the rest Class I.[15]

Why repetitive DNA is essential to genome function 1

The discovery of repetitive DNA presents a conceptual problem for traditional genebased notions of hereditary information. repetitive DNA is an essential component of genomes; it is required for formatting coding information so that it can be accurately expressed and for formatting DNA molecules for transmission to new generations of cells. In addition, the cooperative nature of proteinDNA interactions provides another fundamental reason why repeated sequence elements are essential to format genomic DNA. Instead of parasites, we argue that repetitive DNA elements are necessary organisers of genomic information.

molecular genetics has shown that achieving this task requires cells to possess a number of additional capabilities also encoded in the genome:

(1) Regulating timing and extent of coding sequence expression.
(2) Organizing coordinated expression of protein and RNA molecules that function together.
(3) Packaging DNA appropriately within the cell.
(4) Replicating the genome in synchrony with the cell division cycle.
(5) Transmitting replicated DNA accurately to progeny cells at cell division.
(6) Detecting and repairing errors and damage to the genome.
(7) Restructuring the genome when necessary (as part of the normal life cycle or in response to a critical selective challenge).

These additional capabilities involve specific kinds of interactions between DNA and other cellular molecules. The construction of highly precise transcription
complexes in RNA and protein synthesis is one example of such interactions (Ptashne, 1986). Formation of a kinetochore structure at the centromere for attachment of microtubulues to ensure chromosome distribution at mitosis is another example (Volpe et al., 2003).

The idea that repetitive DNA is ‘junk’ without functional significance in the genome is simply not consistent with an extensive and growing literature, only a minor part of which is cited here.

Transposable elements CONTAIN SIGNALS that define the boundaries of each element and help create nucleoprotein structures that allow them to interact with and rearrange target DNA sequences [e.g. terminal inverted repeats (TIRs) of DNA transposons and long terminal repeats (LTRs) in retrotransposons (Craig et al., 2002)]. In addition, transposons and retrotransposons CONTROL SEQUENCE COMPONENTS that control transcription and may participate in DNA replication and chromatin organisation. We know from an extensive literature on insertional mutagenesis in nature and the laboratory that introduction of a transposable element into a particular location CONFERS NEW FUNCTIONAL PROPERTIES on that region of the genome (Shapiro, 1983; Craig et al., 2002; Deininger et al., 2003).

Since gypsy and other mobile elements retain their structures as they migrate through the genome, there is predictability to the signals they will carry with them. Thus, cells have the ability to introduce a PREORGANISED CONSTELLATION OF FUNCTIONAL SIGNALS  into any location in the genome.

The notion that LINE elements are MAJOR ORGANISERS  of genome functional architecture is supported by close comparative analysis of syntenic regions in the mouse and human genomes.


Primate specific retrotransposons, SVAs, in the evolution of networks that alter brain function. 2
Our analysis suggests a potential role of SVAs in evolution of human CNS and especially emergence of functional trends relevant to social and parental behaviour. It also supports models which explain in part how brain function can be modulated by both the immune and reproductive systems based on the gene expression patterns and gene pathways potentially altered by SVA insertions.

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2 Re: Transposons and Retrotransposons on Fri Dec 16, 2016 6:00 pm



We have seen that homologous recombination can result in the exchange of DNA sequences between chromosomes. However, the order of genes on the interacting chromosomes typically remains the same following homologous recombination, inasmuch as the recombining sequences must be very similar for the process to occur. We will describe two very different types of recombination—transposition (also called transpositional recombination) and conservative site-specific recombination—that do not require substantial regions of DNA homology. These two types of recombination reactions can alter gene order along a chromosome and can cause unusual types of mutations that introduce whole blocks of DNA sequence into the genome.

Transposition and conservative site-specific recombination are largely dedicated to moving a wide variety of specialized segments of DNA—collectively termed mobile genetic elements—from one position in a genome to another. We will see that mobile genetic elements can range in size from a few hundred to tens of thousands of nucleotide pairs, and each typically carries a unique set of genes. Often, one of these genes encodes a specialized enzyme that catalyzes the movement of only that element, thereby making this type of recombination possible. Virtually all cells contain mobile genetic elements (known informally as “jumping genes”). Over evolutionary time scales, they have had a profound effect on the shaping of modern genomes. For example, nearly half of the human genome can be traced to these elements (see Figure4–62).

Over time, random mutation has altered their nucleotide sequences, and, as a result, only a few of the many copies of these elements in our DNA are still active and capable of movement. The remainder are molecular fossils whose existence provides striking clues to our evolutionary history.

Thats a highly questionable assertion.....

Mobile genetic elements are often considered to be molecular parasites (they are also termed “selfish DNA”) that persist because cells cannot get rid of them; they certainly have come close to overrunning our own genome. However, mobile DNA elements can provide benefits to the cell. For example, the genes they carry are sometimes advantageous, as in the case of antibiotic resistance in bacterial cells. The movement of mobile genetic elements also produces many of the genetic variants upon which evolution depends, because, in addition to moving themselves, mobile genetic elements occasionally rearrange neighboring sequences of the host genome. Thus, spontaneous mutations observed in Drosophila, humans, and other organisms are often due to the movement of mobile genetic elements. While many of these mutations will be deleterious to the organism, some will be advantageous and may spread throughout the population. It is almost certain that much of the variety of life we see around us originally arose from the movement of mobile genetic elements. In this section, we introduce mobile genetic elements and describe the mechanisms that enable them to move around a genome. We shall see that some of these elements move through transposition mechanisms and others through conservative site-specific recombination. We begin with transposition, as there are many more known examples of this type of movement.

Through Transposition, Mobile Genetic Elements Can Insert Into Any DNA Sequence

Mobile elements that move by way of transposition are called transposons, or transposable elements. In transposition, a specific enzyme, usually encoded by the transposon itself and typically called a transposase, acts on specific DNA sequences at each end of the transposon, causing it to insert into a new target DNA site. Most transposons are only modestly selective in choosing their target site, and they can therefore insert themselves into many different locations in a genome. In particular, there is no general requirement for sequence similarity between the ends of the element and the target sequence. Most transposons move only rarely. In bacteria, where it is possible to measure the frequency accurately, transposons typically move once every 105 cell divisions. More frequent movement would probably destroy the host cell’s genome. On the basis of their structure and transposition mechanism, transposons can be grouped into three large classes: DNA-only transposons, retroviral-like retrotransposons, and nonretroviral retrotransposons. The differences among them are briefly outlined in Table 5–4, and each class will be discussed in turn.

DNA-Only Transposons Can Move by a Cut-and-Paste Mechanism

DNA-only transposons, so named because they exist only as DNA during their movement, predominate in bacteria, and they are largely responsible for the spread of antibiotic resistance in bacterial strains. When antibiotics like penicillin and streptomycin first became widely available in the 1950s, most bacteria that caused human disease were susceptible to them. Now, the situation is different— antibiotics such as penicillin (and its modern derivatives) are no longer effective against many modern bacterial strains, including those causing gonorrhea and bacterial pneumonia. The spread of antibiotic resistance is due largely to genes that encode antibiotic-inactivating enzymes that are carried on transposons (Figure 5–60).

Although these mobile elements can transpose only within cells that already carry them, they can be moved from one cell to another through other mechanisms known collectively as horizontal gene transfer. Once introduced into a new cell, a transposon can insert itself into the genome and be faithfully passed on to all progeny cells through the normal processes of DNA replication and cell division. DNA-only transposons can relocate from a donor site to a target site by cutand- paste transposition (Figure 5–61).

Here, the transposon is literally excised from one spot on a genome and inserted into another. This reaction produces a short duplication of the target DNA sequence at the insertion site; these direct repeat sequences that flank the transposon serve as convenient records of prior transposition events. Such “signatures” often provide valuable clues in identifying transposons in genome sequences. When a cut-and-paste DNA-only transposon is excised from its original location, it leaves behind a “hole” in the chromosome. This lesion can be perfectly healed by recombinational double-strand break repair (see Figure 5–48)

provided that the chromosome has just been replicated and an identical copy of the damaged host sequence is available. Alternatively, a nonhomologous end-joining reaction can reseal the break; in this case, the DNA sequence that originally flanked the transposon is altered, producing a mutation at the chromosomal site from which the transposon was excised (see Figure 5–45). Remarkably, the same mechanism used to excise cut-and-paste transposons from DNA has been found to operate in developing immune systems of
vertebrates, catalyzing the DNA rearrangements that produce antibody and T cell receptor diversity.

Some Viruses Use a Transposition Mechanism to Move Themselves Into Host-Cell Chromosomes

Certain viruses are considered mobile genetic elements because they use transposition mechanisms to integrate their genomes into that of their host cell. However, unlike transposons, these viruses encode proteins that package their genetic information into virus particles that can infect other cells. Many of the viruses that insert themselves into a host chromosome do so by employing one of the first two mechanisms listed in Table 5–4; namely, by behaving like DNA-only transposons or like retroviral-like retrotransposons. Indeed, much of our knowledge of these mechanisms has come from studies of particular viruses that employ them. Transposition has a key role in the life cycle of many viruses. Most notable are the retroviruses, which include the human AIDS virus, HIV. Outside the cell, a retrovirus exists as a single-strand RNA genome packed into a protein shell or capsid along with a virus-encoded reverse transcriptase enzyme. During the infection process, the viral RNA enters a cell and is converted to a double-strand DNA molecule
by the action of this crucial enzyme, which is able to polymerize DNA on either an RNA or a DNA template (Figure 5–62).

The term retrovirus refers to the virus’s ability to reverse the usual flow of genetic information, which normally is from DNA to RNA. Once the reverse transcriptase has produced a double-strand DNA molecule, specific sequences near its two ends are recognized by a virus-encoded  transposase called integrase. Integrase then inserts the viral DNA into the chromosome by a mechanism similar to that used by the cut-and-paste DNA-only
transposons (see Figure 5–61).

A Large Fraction of the Human Genome Is Composed of Nonretroviral Retrotransposons

A significant fraction of many vertebrate chromosomes is made up of repeated DNA sequences. In human chromosomes, these repeats are mostly mutated and truncated versions of nonretroviral retrotransposons, the third major type of transposon (see Table 5–4). Although most of these transposons in the human genome are immobile, a few retain the ability to move. Relatively recent movements of the L1 element (sometimes referred to as a LINE or long interspersed nuclear element) have been identified, some of which result in human disease; for example, a particular type of hemophilia results from an L1 insertion into the gene encoding the blood-clotting protein Factor VIII (see Figure 6–24). Nonretroviral retrotransposons are found in many organisms and move via a distinct mechanism that requires a complex of an endonuclease and a reverse transcriptase. As illustrated in Figure 5–63, the RNA and reverse transcriptase have a much more direct role in the recombination event than they do in the retroviral- like retrotransposons described above. Inspection of the human genome sequence reveals that the bulk of nonretroviral retrotransposons—for example, the many copies of the Alu element, a member of the SINE (short interspersed nuclear element) family—do not carry their own endonuclease or reverse transcriptase genes. Nonetheless, they have successfully amplified themselves to become major constituents of our genome, presumably by pirating enzymes encoded by other transposons. Together the LINEs
and SINEs make up over 30% of the human genome
(see Figure 4–62); there are 500,000 copies of the former and over a million of the latter.

At present, we can only wonder how many of our uniquely human qualities arose from the past activity of the many mobile genetic elements whose remnants are found today scattered throughout our chromosomes.

many of the new arrangements of DNA sequences that their site-specific recombination events produce have played an important part in creating the genetic variation crucial for the evolution of cells and organisms.

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3 Human Endogenous Retroviruses (HERVs) on Sat Dec 17, 2016 12:34 pm


Human Endogenous Retrovirus transposable elements (HERVs) 1

Retroelements constitute a large portion of our genomes. One class of these elements, the human endogenous retroviruses (HERVs), is comprised of remnants of ancient exogenous retroviruses that have gained access to the germ line. After integration, most proviruses have been the subject of numerous amplifications and have suffered extensive deletions and mutations. Nevertheless, HERV-derived transcripts and proteins have been detected in healthy and diseased human tissues, and HERV-K, the youngest, most conserved family, is able to form virus-like particles. Although it is generally accepted that the integration of retroelements can cause significant harm by disrupting or disregulating essential genes, the role of HERV expression in the etiology of malignancies and autoimmune and neurologic diseases remains controversial. In recent years, striking evidence has accumulated indicating that some proviral sequences and HERV proteins might even serve the needs of the host and are therefore under positive selection. The remarkable progress in the analysis of host genomes has brought to light the significant impact of HERVs and other retroelements on genetic variation, genome evolution, and gene regulation.

retroviral sequences are involved in the regulation of cellular proteins, as in the liver, placenta, colon etc. 

Histone H3.3 is required for endogenous retroviral element silencing in embryonic stem cells

transposable elements themselves can act as alternative promoters for nearby genes, resulting in non-canonical regulation of transcription

Is there a role for endogenous retroviruses to mediate long-term adaptive phenotypic response upon environmental inputs?

Endogenous retroviruses (ERVs) are long terminal repeat-containing virus-like elements that have colonized approximately 10 per cent of the present day mammalian genomes. The intracisternal A particles (IAPs) are a class of ERVs that is currently highly active in the rodents. IAP elements can influence the transcription profile of nearby genes by providing functional promoter elements and modulating local epigenetic landscape through changes in DNA methylation and histone (H3K9) modifications. Despite the potential role for IAPs in gene regulation, the precise genomic locations where these elements are integrated are not well understood. To address this issue, we have identified more than 400 novel IAP insertion sites within/near annotated genes by searching the murine genome, which suggests that the impact of IAP elements on local and/or global gene regulation could be more profound than was previously expected. On the basis of our independent analyses and already published reports, here we argue that IAPs and ERV elements in general could have an evolutionary role for modulating phenotypic plasticity upon environmental inputs, and that this could be mediated through specific stages of embryonic development such as placentation during which the epigenetic constraints on IAP elements are partially relaxed.


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Transposons are very similar to viruses.  However, they lack genes for viral coat proteins, cannot cross cellular boundaries, and thus they replicate only in the genome of their host.  They can be thought of as intragenomic parasites.  Except in the rarest of circumstances, the only mode of transmission from one metazoan organism to another is directly by DNA duplication and inheritance (e.g. your transposons are given to your children) (Li 1997, pp. 338-345).

Replication for a transposon means copying itself and inserting the copied DNA randomly somewhere else in the host’s genome. . . .

Finding the same transposon in the same chromosomal location in two different species is strong direct evidence of common ancestry, since they insert randomly and generally cannot be transmitted except by inheritance.  In addition, once a common ancestor has been postulated that contains this transposition, all the descendants of this common ancestor should also contain the same transposition.  A possible exception is if this transposition were removed due to a rare deletion event; however, deletions are never clean and usually part of the transposon sequence remains.

Presumably, the alleged prediction and fulfillment are:

If universal common ancestry is true, then the same transposon will exist in the same chromosomal location in two or more species.

The same transposon exists in the same chromosomal location in two or more species.

It is not a prediction of the hypothesis of universal common ancestry or the more specific hypothesis of Neo-Darwinism that the “same transposon”[39] will exist in the same chromosomal location in two or more species.  Evolution does not even predict the existence of transposons, much less that they will be found at the same location in two or more species.  Until transposons were discovered in the late 1940s, conventional wisdom was that all genes worked from a stable position along a chromosome, and no one considered that cause for concern.  On the contrary, McClintock’s initial claims about transposons were resisted because they were contrary to the prevailing view of genetics.  So, while evolutionary theory was able to accommodate transposons, it was quite comfortable with their absence.

Evolution likewise makes no prediction about how transposons will operate, given their existence.  The theory can accommodate any process of transposition, however simple or complex and however chaotic or uniform, and can accommodate the transposed elements remaining at insertion sites for any length of time.  Thus, transposons are not confirmation of an evolutionary prediction but observations that are given an evolutionary interpretation.

Moreover, transposons are inadequate in principle to support Dr. Theobald’s claim of universal common ancestry, because they are not shared by all groups of organisms.  As Edward Max acknowledges (in Sec. 4.7 of the online article cited by Dr. Theobald), “Another limitation [of this argument] is that there are no examples of ‘shared errors’ that link mammals to other branches of the genealogic tree of life on earth. . . .  Therefore, the evolutionary relationships between distant branches on the evolutionary genealogic tree must rest on other evidence besides ‘shared errors.’”

The claim here is that common ancestry is the only viable explanation for the same transposon being at the same locus in separate species.  It is based on the premise that transposons are (and always have been) nonfunctional products of genetic accidents that insert randomly into the genome of the host organism.  The presumed nonfunctionality of transposons is thought to eliminate the explanation of design (because a Designer could have no purpose in placing nonfunctional sequences at the same locus in separate species).  The presumed randomness of transposon insertion is thought to eliminate the explanation of chance (because the DNA “chain” is too long for coincidental insertion at the same locus to be a realistic possibility).  That leaves common ancestry as the last explanation standing.

Two considerations undermine this claim.  First, it is an unprovable theological assertion that God would not place nonfunctional sequences at the same locus in separate species.  God may have a purpose for doing so that is beyond our present understanding.  Gibson writes:

The argument that God would not act in a certain way is a theological argument, and can hardly be addressed by science.  The validity of such an argument depends on the kind of God being postulated. The kind of God at issue for most of those involved in this discussion is the God who revealed Himself in the Bible.  The question then is: What do the scriptures say about whether God would create structures or DNA sequences for which we can find no use in unrelated organisms?  This subject is not addressed in the Bible, leaving us without an answer.  We can postulate that God would not do such a thing, but this position would not be based on any evidence other than our own presuppositions, however reasonable they seem.  (Gibson, 100.)

The suggestion that God could not place nonfunctional sequences at the same locus in separate species because that would make him guilty of deception is patently theological.  It is also incorrect.  God cannot be charged fairly with deception when we choose to draw conclusions from data that contradict what he has revealed in Scripture.  To quote Gibson again:

The Scriptures do state clearly that God does not deceive us (Titus 1:2), but they also make it clear that we are naturally prone to make wrong conclusions (Romans 11:33-36).  The Scriptures reveal the truth about history.  When God tells us in Scripture that he created in a certain way, we need not be deceived by what we believe to be appearances to the contrary.  (Gibson, 100.)

Second, even the staunchest critics of creation theory recognize that “[i]t is impossible to prove absence of function for any region of DNA.”[40]  As molecular biologist Carl Schmid puts it, “We know there’s a lot of DNA that we don’t know its function.  The fact that we don’t know its function doesn’t mean it doesn’t have a function.”[41]  The recent indication from the Human Genome Project that the way genes work is “far more complicated than the mechanism long taught” only increases the possibility that seemingly useless DNA has an unknown function.

The issue of function is, of course, much more complex than determining whether a given sequence codes for a product in a laboratory.  To repeat a quote from Jerlstrom:

Failure to observe a pseudogene coding for a product under experimental conditions is no proof that they never do so inside an organism.  It is also impossible to rule out protein expression based solely on sequence information, as DNA messages can be altered by, e.g. editing the transcribed RNA, skipping parts of the sequence, etc.  Moreover, the inability to code for a protein useful to an organism hardly exhausts other possible functions pseudogenes may have.  (Jerlstrom, 15.)

Walkup says of transposons (and the other major kinds of “junk DNA”), “Recent research has begun to show that many of these useless-looking sequences do have a function.” (Walkup, 19.) According to Woodmorappe, who cites a forthcoming paper by Paul Nelson and others, “[E]vidence for function is not limited to generic ‘junk DNA’, but is now known for representatives of all major types of pseudogenes.”[42] (Woodmorappe 2000, 57.)

Regarding the Alu element cited by Dr. Theobald as an illustrative transposon, Jerlstrom writes, “[T]here is a growing body of evidence that Alu (a SINE) sequences are involved in gene regulation, such as in enhancing and silencing gene activity, or can act as a receptor-binding site—this is surely a precedent for the functionality of other types of pseudogenes.” (Jerlstrom, 15.)  Woodmorappe reports that “[t]he functionality of Alu units has long been suspected, and recently confirmed.” (Woodmorappe 2000, 57; see also, Walkup, 23.)

Of course, if transposons have a function, then God may have had a functional reason for initially placing them at the same chromosomal location in separately created species.  He also may have had a functional reason for designing certain transposons with an insertion bias for certain loci.

As mentioned previously, geneticist Todd Wood proposes that God endowed creatures with mobile genetic elements (which he calls Altruistic Genetic Elements) to facilitate diversification within created kinds (see, Walkup, 26-27).[43]  Since the Fall, this complex diversification system is believed to have degenerated so that only remnants and distortions of its past operation are available to us today.  If that is correct, the fact we do not see insertion bias in a particular transposon, for example, does not mean that it never existed.  And the insertion bias that we do observe in some transposons (see, e.g., Walkup, 25; Woodmorappe 2000, 63-64) may no longer be serving its original purpose.

The evolutionary belief that transposons have remained recognizable for eons supports the view that they are (or have been) functional.  Woodmorappe writes, “[O]rthologous SINEs have now been found in different phyla, and the cited researchers recognize that the (evolutionary) maintenance of a close correspondence between such phylogenetically-distant organisms is very difficult to explain if SINEs are of no use to their carriers.” (Woodmorappe 2000, 58.)  To repeat another quote from Jerlstrom:

The persistence of pseudogenes [including transposons] is in itself additional evidence for their activity.  This is a serious problem for evolution, as it is expected that natural selection would remove this type of DNA if it were useless, since DNA manufactured by the cell is energetically costly.  Because of the lack of selective pressure on this neutral DNA, one would also expect that ‘old’ pseudogenes should be scrambled beyond recognition as a result of accumulated random mutations.  Moreover, a removal mechanism for neutral DNA is now known.  (Jerlstrom, 15.)

Interestingly, one of the ways evolutionists explain how the various kinds of transposons spread from the individuals in whose germline cells they first arose to all members of the species is by appeal to the possibility that each of the transposons wound up close to an advantageous gene that became prevalent in the population by natural selection.[44]  In other words, the various transposons are thought to have spread within the originating species by a fortuitous proximity to advantageous genes.  One could turn that around and suggest that the transposons were close to genes because they performed a function related to the genes.  Indeed, the proximity of Alu elements to genes is accepted as evidence that the Alu elements are functional.

[Eric] Lander [a geneticist at M.I.T.] said that in 1998, Carl Schmid, a molecular biologist at the University of California at Davis, advanced what seemed like a nutty idea to explain Alu’s unusual affinity for genes.  Schmid suggested Alu sequences resided near genes because they weren’t junk, but rather a mechanism to help cells repair themselves.

With the entire genome map in front of them, showing so many instances of Alu sequences around genes, scientists are beginning to take Schmid seriously.  “It looks pretty convincing,” [Francis] Collins said.[45]

One need not be a creationist to doubt the claim that shared transposons are sufficient to establish common ancestry.  Regarding the very transposons cited by Dr. Theobald as proof of the common ancestry of whales, hippos, and ruminants, noted vertebrate paleontologist Maureen O’Leary recently rebuked Okada for rejecting the possibility that SINEs and LINEs could arise independently in separate lineages (i.e., evolve convergently).  Gura reports:

Okada’s studies on SINEs and LINEs, held up by the molecular enthusiasts as their strongest line of evidence, have attracted particular scrutiny.  “It is an outdated method in systematics to assert that one aspect of the organism somehow dictates the true phylogeny,” says O’Leary.  “Okada is approaching this completely backwards by asserting that his retrotransposons are so significant that he cannot imagine a way in which they evolved convergently.” (Gura, 232.)

Even more recently, a team of molecular geneticists discovered two “hot spots” where the same SINEs inserted independently.  They write:

Vertebrate retrotransposons have been used extensively for phylogenetic analyses and studies of molecular evolution. Information can be obtained from specific inserts either by comparing sequence differences that have accumulated over time in orthologous copies of that insert or by determining the presence or absence of that specific element at a particular site.  The presence of specific copies has been deemed to be an essentially homoplasy-free phylogenetic character because the probability of multiple independent insertions into any one site has been believed to be nil. . . . We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites.  These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry.  Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.  (Cantrell and others, 769.)


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Epigenetic regulation of transcription and possible functions of mammalian short interspersed elements, SINEs

Despite intensive studies on human and mouse SINEs, the mysteries of their genomic distribution and evolutionary dynamics remain unsolved. Moreover, many other mammalian SINEs are yet uncharacterized in terms of transcription and function. Therefore, future research directions would be toward understanding how Pol III and TFIIIC binding is regulated, what molecules are involved in SINE-derived enhancers and chromatin boundaries, how SINE retrotransposition is regulated in the germline and early development, and to what extent the proposed functions are conserved or diverged in a wide variety of mammalian and non-mammalian SINEs. It is undoubted that epigenetic regulation will be the pivot for these studies.


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6 Re: Transposons and Retrotransposons on Thu Mar 09, 2017 5:09 pm



Transposable elements just don’t make sense. These so-called “jumping genes” are segments of junk DNA that insert themselves at random in our genomes. That is the evolutionary interpretation of these genetic units, but how and why do they move about, and why don’t they wreak havoc on the genome? The answers to these questions, which have been emerging in recent years, is that transposable elements are exquisite, finely-tuned, highly-functional molecular machines that contradict evolutionary expectations. Evolutionists have a long, failed history of presumed disutility—after all, the world arose by chance, surely it doesn’t work very well—and transposable elements are just one more example of this failed prediction. But the junk-to-hero story is only one of three ways that transposable elements utterly demolish evolutionary theory. The other two prongs in this Darwin-destroying triad are serendipity and pattern.

By serendipity, I am referring to the rather awkward findings, which are undeniable at this point, that if evolution is true, then it must have come about by highly complex, non adaptive, mechanisms. From diploid genetics to horizontal gene transfer, alternate gene splicing, genetic regulation, epigenetics, mechanisms that cause adaptive mutations, and transposable elements, evolution must have bumbled along by luckily constructing fantastically complex mechanisms. Those mechanisms would provide no immediate adaptive value, yet somehow would persist and become vital agents in evolutionary history. Simply put, evolution must have created evolution in a most unlikely (astronomically unlikely) set of circumstances. That’s serendipity, not science, and transposable elements heaps more fuel onto the fire.

By pattern, I am referring to another set of awkward findings, again undeniable, that the pattern of structures observed across the species consistently contradicts evolution’s predictions. One of those contradictions are the enormous differences found in otherwise allied species.

All three of these contradictions—disutility, serendipity, and pattern—are on display this week in new, systematic study of transposable elements out of Didier Trono’s lab in Switzerland. The study details the interactions between transposable elements and a class of proteins. The findings indicate the complexity and interdependency of these molecular mechanisms. As the press release admits:

Long considered as junk DNA, transposable elements are now recognized as influencing the expression of genes. … the extent of this regulation and how it is harnessed were so far unknown. EPFL scientists have now taken the first extensive look at a family of ~350 human proteins, showing that they establish a complex interplay with transposable elements … KZFPs can convert transposable elements in exquisitely fine-tuned regulatory platforms that influence the expression of genes, which likely takes place at all stages of development and in all human tissues. … It is a highly combinatorial and versatile system … As a field, epigenetics has come into prominence in recent years, revealing a previously unimagined complexity and elegance in genetics.

Not exactly junk DNA. And of course all of this would require large amounts of serendipity. For evolutionists are now forced to say that transposable elements would have to have played a, err, key role in evolution itself. Evolution would have had to have constructed this highly specific, detailed, system including hundreds of proteins and genetic elements, with hundreds of specific interactions, providing no immediate benefit. As Trono explains:

The vast majority of KZFPs binds to specific motifs in transposable elements. For each KZFP we were able to assign one subset of transposable elements, and also found that one transposable element can often interact with several KZFPs.

Finally, all of this contradicts the expected common descent pattern. This failure has become so common we now have non evolutionary terminology, such as “species-specific” and “lineage-specific.” The paper uses the term “species-restricted”:

KZFPs partner with transposable elements to build a largely species-restricted layer of epigenetic regulation

Species-restricted? In other words, the designs we are discovering in biology are unique to particular species. This is precisely the opposite of what evolution expects. Note also the teleological language (which as usual is evident in the infinitive form): The proteins “partner” with the transposable elements “to build” a largely “species-restricted” layer of epigenetic regulation. This is a classic example of evolution’s absurd creation story language.

The contradictory pattern was, of course, unsuspected. As Trono explains:

KZFPs contribute to make human biology unique. Together with their genomic targets, they likely influence every single event in human physiology and pathology, and do so by being largely species-specific -- the general system exists in many vertebrates, but most of its components are different in each case. … This paper lifts the lid off something that had been largely unsuspected: the tremendous species-specific dimension of human gene regulation.

Yes, it was largely unsuspected. For what these findings reveal is a tremendous species-specific dimension of human gene regulation. In other words, we would need proteins and genetic elements to evolve, via independent and yet interdependent, random mutations, to construct an entirely new set of genetic regulation instructions. This is astronomically unlikely, no matter how many millions of years are available. From a scientific perspective, these findings demolish evolution.

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7 Re: Transposons and Retrotransposons on Fri Mar 10, 2017 4:20 am


With the sequencing of the human genome, it became clear that jumping genes—mobile genetic elements first discovered in maize by Barbara McClintock in the early 1950s—were also present and highly active during human evolution. About half of the human genome resulted from sequences of genetic code that moved or insert extra copies of themselves throughout the genome.
The evolutionary importance of jumping genes was highlighted by the results of another recent study by Gage and collaborators at Stanford. The research used stem cell technologies developed in Gage's lab to explore how differences in gene expression contribute to human and chimp facial structure. The findings, also reported in Cell, suggested that jumping genes played a role in the evolutionary split between humans and other primates.

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8 Re: Transposons and Retrotransposons on Wed Mar 29, 2017 7:29 am


Goodbye junk-dna!…/goodbye-junk-d…

'Jumping genes' and transposons are cut or silenced by clever mechanisms
Eukaryotic cells are able to produce even thousands of different proteins from one gene. This is why there are even two millions of different proteins in a human body, although there are only about 19,600 protein coding genes used for human cells to produce the huge number of different proteins. This clever mechanism is called alternative splicing. RNA-mediated mechanism uses a gene like a library; it makes a template and modifies it by several ways. Cutting, pasting, recombining, moving, removing etc.
Sometimes some strands (rna-like tetrotransposos) needed for the alternative splicing mechanism are inserted into the genome by mistake. These genomic parasites can be harmful for genomic stability and integrity. Especially in germline cells they can cause serious troubles, even cell death. That's why there are mechanisms designed in the cell, that silence or remove those erroneous genetic sequences. The mechanism is described here:…/transcription-mechanism-sheds-li…

Excerpt: "The researchers have found that small pieces of RNA get stitched together into a loop. The investigators were interested in the unicellular ciliate, Paramecium tetraurelia, because they identified small RNA molecules that excise pieces of Paramecium DNA. Looking deeper, there was a kind of feedback loop operating in the excision of DNA segments. Junk DNA was being cut out of the genome, and it is then transcribed into RNA before getting degraded by cellular machinery. The transcribed RNAs act to help cut out even more DNA, building up the RNA production from these excised pieces. However, the resulting RNA pieces are quite small; they are too tiny to be read by normal cellular machinery.
The scientists had to keep digging to learn more about what as happening. "It was an interesting detective work," Nowacki remembers. They had a suspect -- all they needed was to pin it down. "We were not actually looking for the unknown, because we soon had an idea, and then it was all about testing that idea." What they found was that the RNAs were strung together, into strands or concatemers that are about 200 base pairs long and then closed into a loop.
The evidence continues to mount that so-called junk DNA has important functions, likely in the regulation of gene expression and who knows what else. Nowacki suggested that this is the first time, a precise mechanism has been identified whereby deleted, junk DNA is transcribed. That could mean it will finally shed its junky nickname.
Nowacki's lab is working on the NCCR "RNA & Disease -- The Role of RNA Biology in Disease Mechanisms" project, which aims to reveal more about the role of RNA in disease. RNA is a crucial part of gene expression, and disruptions in that system have been linked to cancer, diseases of the heart and brain, and metabolic disorders. Swiss researchers that study different aspects of the function and characteristics of RNA work together at the NCCR, coordinating research using a variety of models like plants, yeast, roundworms, mice and human cells."
My comment: The cell uses mistakes for finding more mistakes! An incredible mechanism! There are no selfish genes or jumping genes. Unchecked, unremoved or unsilenced transposons typically cause diseases. Modern science has just found out the link between the ALS disease and unsilenced dna-transposons:…/…

There are no mechanisms for assumed evolution. Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.

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The impact of retrotransposons on human genome evolution 1

Non-LTR retrotransposons – including LINE-1 (or L1), Alu and SVA elements – have proliferated during the past 80 million years of primate evolution and now account for approximately one third of the human genome. These transposable elements are now known to affect the human genome in many different ways: generating insertion mutations, genomic instability, alterations in gene expression and also contributing to genetic innovation. As the sequences of human and other primate genomes are analyzed in increasing detail, we are begining to understand the scale and complexity of the past and current contribution of non-LTR retrotransposons to genomic change in the human lineage.

Junk DNA' defines differences between humans and chimps 2

For years, scientists believed the vast phenotypic differences between humans and chimpanzees would be easily explained – the two species must have significantly different genetic makeups. However, when their genomes were later sequenced, researchers were surprised to learn that the DNA sequences of human and chimpanzee genes are nearly identical. What then is responsible for the many morphological and behavioral differences between the two species? Researchers at the Georgia Institute of Technology have now determined that the insertion and deletion of large pieces of DNA near genes are highly variable between humans and chimpanzees and may account for major differences between the two species.


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10 ALUternative Regulation for Gene Expression on Tue Apr 11, 2017 4:22 pm


ALUternative Regulation for Gene Expression

Alu elements belong to the primate-specific SINE family of retrotransposons and constitute almost 11% of the human genome, with >1 million copies, and their genomic distribution is biased toward gene-rich regions. Alus are transcribed by RNA polymerase (Pol) III and are inserted back into the genome with the help of autonomous LINE retroelements. Since Alu elements are preferentially located near to or within gene-rich regions, they can affect gene expression by distinct mechanisms of action at both DNA and RNA levels. In this review we focus on recent advances of how Alu elements are pervasively involved in gene regulation. We discuss the impacts of Alu DNA sequences that are in close proximity to genes, Pol-III-transcribed free Alu RNAs, and Pol-II-transcribed Alu RNAs that are embedded within coding or noncoding RNA transcripts. The recent elucidation of Alu functions reveals previously underestimated roles of these selfish or junk DNA sequences in the human genome.
Primate-specific Alus constitute 11% of the human genome, with >1 million copies, and their genomic distribution is biased toward gene-rich regions.
The functions of Alus are highly associated with their sequence and structural features.
Alus can regulate gene expression by serving as cis elements.
Pol-III-transcribed free Alus mainly affect Pol II transcription and mRNA translation in trans.
Embedded Alus within Pol-II-transcribed mRNAs can impact their host gene expression through the regulation of alternative splicing, and RNA stability and translation.
Nearly half of annotated Alus are located in introns; RNA pairing formed by orientation-opposite Alus across introns promotes circRNA biogenesis.

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