Transposons: The Jumping Genes
By: Leslie A. Pray, Ph.D. © 2008 Nature Education
Citation: Pray, L. (2008) Transposons: The jumping genes. Nature Education 1(1):204
Transposable elements, or "jumping genes", were first identified by Barbara McClintock more than 50
years ago. Why are transposons so common in eukaryotes, and exactly what do they do?
Transposable elements (TEs), also known as "jumping genes," are DNA sequences that move from one
location on the genome to another. These elements were first identified more than 50 years ago by
geneticist Barbara McClintock of Cold Spring Harbor Laboratory in New York. Biologists were
initially skeptical of McClintock's discovery. Over the next several decades, however, it became
apparent that not only do TEs "jump," but they are also found in almost all organisms (both
prokaryotes and eukaryotes) and typically in large numbers. For example, TEs make up approximately
50% of the human genome and up to 90% of the maize genome (SanMiguel, 1996).
Types of Transposons
Today, scientists know that there are many different types of TEs, as well as a number of ways to
categorize them. One of the more common divisions is between those TEs that require reverse
transcription (i.e., the transcription of RNA into DNA) in order to transpose and those that do not. The
former elements are known as retrotransposons or class 1 TEs, whereas the latter are known as DNA
transposons or class 2 TEs. The Ac/Ds system that McClintock discovered falls in the latter category.
Different classes of transposable elements are found in the genomes of different eukaryotic organisms
(Figure 1).
Figure 1: The relative amount of retrotransposons and DNA transposons in diverse eukaryotic
genomes. This graph shows the contribution of DNA transposons and retrotransposons in percentage
relative to the total number of transposable elements in each species. (Sc: Saccharomyces cerevisiae;
Sp: Schizosaccharomyces pombe; Hs: Homo sapiens; Mm: Mus musculus; Os: Oryza sativa; Ce:
Caenorhabditis elegans; Dm: Drosophila melanogaster; Ag: Anopheles gambiae, malaria mosquito;
Aa: Aedes aegypti, yellow fever mosquito; Eh: Entamoeba histolytica; Ei: Entamoeba invadens; Tv:
Trichomonas vaginalis.) © 2007 Annual Reviews Feschotte, C. & Pritham, E. J. DNA transposons and
the evolution of eukaryotic genomes. Annual Reviews in Genetics 41, 331–348. All rights reserved.
DNA Transposons
All complete or "autonomous" class 2 TEs encode the protein transposase, which they require for
insertion and excision (Figure 2). Some of these TEs also encode other proteins. Note that DNA
transposons never use RNA intermediaries—they always move on their own, inserting or excising
themselves from the genome by means of a so-called "cut and paste" mechanism.
Figure 2: Classes of mobile elements. DNA transposons (e.g., Tc-1-mariner) have inverted terminal
inverted repeats (ITRs) and a single open reading frame (ORF) that encodes a transposase. They are
flanked by short direct repeats (DRs). Retrotransposons are divided into autonomous and
nonautonomous classes depending on whether they have ORFs that encode proteins required for
retrotransposition. Common autonomous retrotransposons are (i) LTRs or (ii) non-LTRs. Examples of
LTR retrotransposons are human endogenous retroviruses (HERV) (shown) and various Ty elements
of S. cerevisiae (not shown). These elements have terminal LTRs and slightly overlapping ORFs for
their group-specific antigen (gag), protease (prt), polymerase (pol), and envelope (env) genes. They
produce target site duplications (TSDs) upon insertion. Also shown are the reverse transcriptase (RT)
and endonuclease (EN) domains. Other LTR retrotransposons that are responsible for most mobileelement insertions in mice are the intracisternal A-particles (IAPs), early transposons (Etns), and
mammalian LTR-retrotransposons (MaLRs). These elements are not present in humans, and
essentially all are defective, so the source of their RT in trans remains unknown. L1 is an example of a
non-LTR retrotransposon. L1s consist of a 5'-untranslated region (5' UTR) containing an internal
promoter, two ORFs, a 3' UTR, and a poly(A) signal followed by a poly(A) tail (An). L1s are usually
flanked by 7- to 20-bp target site duplications (TSDs). The RT, EN, and a conserved cysteine-rich
domain (C) are shown. An Alu element is an example of a nonautonomous retrotransposon. Alus
contain two similar monomers, the left (L) and the right (R), and end in a poly(A) tail. Approximate
full-length element sizes are given in parentheses. © 2004 American Association for the Advancement
of Science Kazasian, H. H. Mobile elements: drivers of genome evolution. Science 303, 1626–1632
(2004). All rights reserved.
Class 2 TEs are characterized by the presence of terminal inverted repeats, about 9 to 40 base pairs
long, on both of their ends (Figure 3). As the name suggests and as Figure 3 shows, terminal inverted
repeats are inverted complements of each other; for instance, the complement of ACGCTA (the
inverted repeat on the right side of the TE in the figure) is TGCGAT (which is the reverse order of the
terminal inverted repeat on the left side of the TE in the figure). One of the roles of terminal inverted
repeats is to be recognized by transposase.
Figure 3: The structure of a DNA transposon.
DNA transposons, also known as class 2 transposable elements, are flanked at both ends by terminal
inverted repeats. The inverted repeats are complements of each other (the repeat at one end is a mirror
image of, and composed of complementary nucleotides to, the repeat at the opposing end). © 2013
Nature Education Adapted from Pierce, Benjamin. Genetics: A Conceptual Approach, 2nd ed. All
rights reserved.
In addition, all TEs in both class 1 and class 2 contain flanking direct repeats (Figure 3). Flanking
direct repeats are not actually part of the transposable element; rather, they play a role in insertion of
the TE. Moreover, after a TE is excised, these repeats are left behind as "footprints." Sometimes, these
footprints alter gene expression (i.e., expression of the gene in which they have been left behind) even
after their related TE has moved to another location on the genome.
Less than 2% of the human genome is composed of class 2 TEs. This means that the majority of the
substantial portion of the human genome that is mobile consists of the other major class of TEs—the
retrotransposons (Kazazian & Moran, 1998).
Retrotransposons
Unlike class 2 elements, class 1 elements—also known as retrotransposons—move through the action
of RNA intermediaries. In other words, class 1 TEs do not encode transposase; rather, they produce
RNA transcripts and then rely upon reverse transcriptase enzymes to reverse transcribe the RNA
sequences back into DNA, which is then inserted into the target site.
There are two major types of class 1 TEs: LTR retrotransposons, which are characterized by the
presence of long terminal repeats (LTRs) on both ends; and non-LTR TEs, which lack the repeats.
Both the LINE1, or L1, and Alu genes represent families of non-LTR TEs. L1 elements average about 6
kilobases in length. In contrast, Alu elements average only a few hundred nucleotides, thus making
them a short interspersed transposable element, or SINE. Alu is particularly prolific, having originated
in primates and expanding in a relatively short time to about 1 million copies per cell in humans. L1 is
also common in humans; although not present in as many copies as Alu, its larger size means that this
element makes up an estimated 15%–17% of the human genome (Kazazian & Moran, 1998; Slotkin &
Martienssen, 2007). In humans, these non-LTR TEs are the only active class of transposons; LTR
retrotransposons and DNA transposons are only ancient genomic relics and are not capable of
jumping.
Autonomous and Nonautonomous Transposons
Both class 1 and class 2 TEs can be either autonomous or nonautonomous. Autonomous TEs can move
on their own, while nonautonomous elements require the presence of other TEs in order to move. This
is because nonautonomous elements lack the gene for the transposase or reverse transcriptase that is
needed for their transposition, so they must "borrow" these proteins from another element in order to
move. Ac elements, for example, are autonomous because they can move on their own, whereas Ds
elements are nonautonomous because they require the presence of Ac in order to transpose.
What Jumping Genes Do (Besides Jump)
The fact that roughly half of the human genome is made up of TEs, with a significant portion of them
being L1 and Alu retrotransposons, raises an important question: What do all these jumping genes do,
besides jump? Much of what a transposon does depends on where it lands. Landing inside a gene can
result in a mutation, as was discovered when insertions of L1 into the factor VIII gene caused
hemophilia (Kazazian et al., 1988). Similarly, a few years later, researchers found L1 in the APC genes
in colon cancer cells but not in the APC genes in healthy cells in the same individuals. This confirms
that L1 transposes in somatic cells in mammals, and that this element might play a causal role in
disease development (Miki et al., 1992).
Silencing and Transposons
As opposed to L1, most TEs appear to be silent—in other words, these elements do not produce a
phenotypic effect, nor do they actively move around the genome. At least that has been the general
scientific consensus. Some silenced TEs are inactive because they have mutations that affect their
ability to move from one chromosomal location to another; others are perfectly intact and capable of
moving but are kept inactive by epigenetic defense mechanisms such as DNA methylation, chromatin
remodeling, and miRNAs. In chromatin remodeling, for example, chemical modifications to the
chromatin proteins cause chromatin to become so constricted in certain areas of the genome that the
genes and TEs in those areas are silenced because transcription enzymes simply cannot access them.
Another example of transposon silencing involves plants in the genus Arabidopsis. Researchers who
study these plants have found they contain more than 20 different mutator transposon sequences (a
type of transposon identified in maize). In wild-type plants, these sequences are methylated, or
silenced. However, in plants that are defective for one of the enzymes responsible for methylation,
these transposons are transcribed. Moreover, several different mutant phenotypes have been explored
in the methylation-deficient plants, and these phenotypes have been linked to transposon insertions
(Miura et al., 2001).
Based on studies such as these, scientists know that some TEs are epigenetically silenced; in recent
years, however, researchers have begun to wonder whether certain TEs might themselves have a role
in epigenetic silencing. Interestingly, it was Barbara McClintock who first speculated that TEs might
play this kind of regulatory role (McClintock, 1951). It has taken decades for scientists to collect
enough evidence to consider that maybe McClintock's speculation had a kernel of truth to it.
Transposons Can Encode siRNAs That Mediate Their Own Silencing
Because transposon movement can be destructive, it is not surprising that most of the transposon
sequences in the human genome are silent, thus allowing this genome to remain relatively stable,
despite the prevalence of TEs. In fact, investigators think that of the 17% of the human genome that is
encoded by L1-related sequences, only about 100 active L1 elements remain. Moreover, research
suggests that even these few remaining active transposons are inhibited from jumping in a variety of
ways that go beyond epigenetic silencing.
For instance, in human cells, small interfering RNAs (siRNAs), also known as RNAi, can prevent
transposition. RNAi is a naturally occurring mechanism that eukaryotes often use to regulate gene
expression. What is especially interesting about this situation is that the siRNAs that interfere with L1
activity are derived from the 5′ untranslated region (5′ UTR) of L1 LTRs. Specifically, the 5′ UTR of
the L1 promoter encodes a sense promoter that transcribes the L1 genes, as well as an antisense
promoter that transcribes an antisense RNA. Yang and Kazazian (2006) demonstrated that this results
in homologous sequences that can hybridize, thereby forming a double-stranded RNA molecule that
can serve as a substrate for RNAi. Furthermore, when the investigators inhibited endogenous siRNA
silencing mechanisms, they saw an increase in L1 transcripts, suggesting that transcription from L1 is
indeed inhibited by siRNA.
Transposons Are Not Always Destructive
Not all transposon jumping results in deleterious effects. In fact, transposons can drive the evolution of
genomes by facilitating the translocation of genomic sequences, the shuffling of exons, and the repair
of double-stranded breaks. Insertions and transposition can also alter gene regulatory regions and
phenotypes. In the case of medaka fish, for instance, the Tol2 DNA transposon is directly linked to
pigmentation. One highly inbred line of these fish was shown to have a variety of pigmentation
patterns. In the members of this line in which the Tol2 transposon hopped out "cleanly" (i.e., without
removing other parts of the genomic sequence), the fish were albino. But when Tol2 did not cleanly
hop from the regulatory region, the result was a wide range of heritable pigmentation patterns (Koga et
al., 2006).
The fact that transposable elements do not always excise perfectly and can take genomic sequences
along for the ride has also resulted in a phenomenon scientists call exon shuffling. Exon shuffling
results in the juxtaposition of two previously unrelated exons, usually by transposition, thereby
potentially creating novel gene products (Moran et al., 1999).
The ability of transposons to increase genetic diversity, together with the ability of the genome to
inhibit most TE activity, results in a balance that makes transposable elements an important part of
evolution and gene regulation in all organisms that carry these sequences.
References and Recommended Reading
Bailey, J. A., et al. Molecular evidence for a relationship between LINE-1 elements and X
chromosome inactivation: The Lyon repeat hypothesis. Proceedings of the National Academy of
Sciences 97, 6634–6639 (2000)
Feschotte, C., et al. Plant transposable elements: Where genetics meets genomics. Nature Reviews
Genetics 3, 329–341 (2002) (link to article)
Kazazian, H. H. Mobile elements: Drivers of genome evolution. Science 303, 1626–1632 (2004)
doi:10.1126/science.1089670
Kazazian, H. H., & Moran, J. V. The impact of L1 retrotransposons on the human genome. Nature
Genetics 19, 19–24 (1998) (link to article)
Kazazian, H. H., et al. Haemophilia A resulting from de novo insertion of L1 sequences represents a
novel mechanism for mutation in man. Nature 332, 164–166 (1988) (link to article)
Koga, A., et al. Vertebrate DNA transposon as a natural mutator: The medaka fish Tol2 element
contributes to genetic variation without recognizable traces. Molecular Biology and Evolution 23,
1414–1419 (2006) doi:10.1093/molbev/msl003
McLean,
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McClintock, B. Mutable loci in maize. Carnegie Institution of Washington Yearbook 50, 174–181
(1951) (link to article)
Miki, Y., et al. Disruption of the APC gene by a retrotransposal insertion of L1 sequence in colon
cancer. Cancer Research 52, 643–645 (1992)
Miura, A., et al. Mobilization of transposons by a mutation abolishing full DNA methylation in
Arabidopsis. Nature 411, 212–214 (2001) (link to article)
Moran, J. V., et al. Exon shuffling by L1 retrotransposition. Science 283, 1530–1534 (1999)
SanMiguel, P., et al. Nested retrotransposons in the intergenic regions of the maize genome. Science
274, 765–768 (1996)
Slotkin, R. K., & Martienssen, R. Transposable elements and the epigenetic regulation of the genome.
Nature Reviews Genetics 8, 272–285 (2007) (link to article)
Yang, N., & Kazazian, H. H. L1 retrotransposition is suppressed by endogenously encoded small
interfering RNAs in human cultured cells. Nature Structural and Molecular Biology 13, 763–771
(2006) (link to article)
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Source: http://www.nature.com/scitable/topicpage/transposons-the-jumping-genes-518
Transposons, or Jumping Genes: Not Junk DNA?
By: Leslie Pray, Ph.D. © 2008 Nature Education
Citation: Pray, L. (2008) Transposons, or jumping genes: Not junk DNA? Nature Education 1(1):32
For decades, scientists dismissed transposable elements, also known as transposons or “jumping
genes”, as useless “junk DNA”. But are they really?
Transposable elements (TEs), also known as "jumping genes" or transposons, are sequences of DNA
that move (or jump) from one location in the genome to another. Maize geneticist Barbara McClintock
discovered TEs in the 1940s, and for decades thereafter, most scientists dismissed transposons as
useless or "junk" DNA. McClintock, however, was among the first researchers to suggest that these
mysterious mobile elements of the genome might play some kind of regulatory role, determining
which genes are turned on and when this activation takes place (McClintock, 1965).
At about the same time that McClintock performed her groundbreaking research, scientists Roy Britten
and Eric Davidson further speculated that TEs not only play a role in regulating gene expression, but
also in generating different cell types and different biological structures, based on where in the genome
they insert themselves (Britten & Davidson, 1969). Britten and Davidson hypothesized that this might
partially explain why a multicellular organism has many different types of cells, tissues, and organs,
even though all of its cells share the same genome. Consider your own body as an example: You have
dozens of different cell types, even though the majority of cells in your body have exactly the same
DNA. If every single gene was expressed in every single one of your cells all the time, you would be
one huge undifferentiated blob of matter!
The early speculations of both McClintock and Britten and Davidson were largely dismissed by the
scientific community. Only recently have biologists begun to entertain the possibility that this socalled "junk" DNA might not be junk after all. In fact, scientists now believe that TEs make up more
than 40% of the human genome (Smit, 1999). It is also widely believed that TEs might carry out some
biological function, most likely a regulatory one—just as McClintock and Britten and Davidson
speculated. Like all scientific hypotheses, however, data from multiple experiments were required to
convince the scientific community of this possibility.
The SINE Superfamily of Transposons
Much of the evidence for the function of TEs comes from the growing realization that many
transposons are highly conserved among distantly related taxonomic groups, suggesting that they must
be of some biological value to the genome (Pennisi, 2007). To say that a DNA sequence is conserved
means that the same TEs, or a family of related TEs, exist in genomes of distantly related species, such
as fish and frogs.
For instance, in one study, Japanese researchers identified a new "superfamily" of TEs (a group of TEs
that share some similarities because of their shared ancestry), which they dubbed V-SINEs. The
scientists then used PCR to show that the V-SINEs were widespread among vertebrates, including
lampreys, cartilaginous fish, bony fish, and amphibians (Ogiwara et al., 2002). Of these vertebrates,
lampreys are the oldest, having emerged in the Cambrian era (544 to 510 million years ago). As the
scientists explained in their paper:
The distribution of V-SINEs suggests that they might have been generated in a common ancestor of
vertebrates and might then have survived in most vertebrates . . . [and] that they might have been
generated in the genome of a common ancestor of vertebrates about 540 million years ago or even
more and might then have survived in most vertebrates until the present day.
These findings suggest that V-SINEs are approximately 540 million years old.
V-SINEs acquired their name from the SINEs, or short interspersed nuclear elements. SINEs are a type
of non-long terminal repeat retrotransposon (non-LTR TE). Like all non-LTR TEs, SINEs (including
V-SINEs) are retrotransposons; this means that their movement around the genome is dependent on the
presence of an RNA intermediary. In this system, the TEs produce RNA transcripts, which are then
converted back into DNA by an enzyme called reverse transcriptase. The new DNA copies then insert
themselves into other spots in the genome.
While the researchers who discovered V-SINEs speculate on their function—specifically, whether they
have something to do with protein production during times of stress, based on the fact that other
researchers have observed greater SINE transcription under stressful conditions—they emphasize that
the true functions of V-SINEs remain a scientific mystery (Ogiwara et al., 2002). The fact that the VSINEs are so highly conserved suggests that, even though their true function is still unknown, these
TEs must have some specific role. If not, then why do so many different species share the same, or
similar, V-SINEs? Over 500 million years is a long time for "junk" to survive if it has no purpose.
Conserved SINE Sequences
Two side-by-side photographs show SINE transposon expression (panel A) and ISL1 gene expression
(panel B) in mouse embryos. In both photographs, the embryos are lightly colored, and a dense,
circular stain is visible in a region near the developing brain. Staining is also present along the length
of each embryo’s dorsal region, near the developing spinal cord. In panel A, the embryo is a
translucent beige color, and the stain appears blue. In panel B, the embryo is an opaque white color,
and the stain appears darker. An arrow in each photograph points to staining around a circular ridge on
each embryo’s left-hand side. An inset photograph in both panels shows the base of the embryo’s
posterior region at a higher magnification. In both embryos, a darkly-stained region of gene activity is
visible at the base of the developing tail.
Figure 1: The SINE transposable element upstream of the ISL1 gene serves to enhance gene expression. A reporter
assay shows that the SINE transposon, when activated, is expressed in the same regions (a) as the ISL1 gene (b). Gene
expression is shown in blue. On the bottom are close-up images of the expression similarities along the geminal eminance.
The arrow points out the staining in the dorsal apical ectodermal ridge. © 2006 Nature Publishing Group Bejerano, G. et al.
A distal enhancer and an ultra conserved exon are derived from a novel retrotransposon. Nature 441, 89 (2006). All rights
reserved.
Other groups of researchers have similarly reported conserved TE sequences among different taxa. For
example, Gill Bejerano and his colleagues (2006) discovered another highly conserved SINE family
when studying the ancient Indonesian coelacanth Latimeria menadoensis. They estimate this SINE
family has been around for at least 410 million years, or since the time when L. menadoensis first
appeared. Bejerano et al. found this conserved TE family, which they named LF-SINE (for lobe-finned
fish or living fossil) not only in modern coelacanths (a type of lobe-finned fish), but also in frogs,
chickens, opossums, dogs, rats, mice, chimps, and humans. Again, these results raise the question of
why, if TEs are indeed "junk," they remained relatively unchanged and still mobile in so many
different taxa over several hundred million years of evolution.
Perhaps even more intriguingly, Bejerano and his colleagues collected data suggesting that the LFSINE family TEs likely play a regulatory role, just as McClintock, Britten, and Davidson suspected
decades ago. First, Bejerano et al. identified a 200-base-pair LF-SINE that resided some 500,000 bases
away from the Isl1 gene, which is active only during motor neuron development. Then, using a
procedure called a mouse enhancer assay, the researchers showed that this TE controlled expression of
Isl1—specifically, only when the TE was turned on was Isl1 turned on. The mouse enhancer assay
involved linking the TE sequence to a gene that would cause cells within a developing mouse embryo
to turn blue when expressed, making the cells readily identifiable (Figure 1). The expression patterns
associated with the color change (and therefore associated with activity of the TE) corresponded to Isl1
expression changes typical of a particular developmental stage, suggesting that the TE functions as an
enhancer, or a regulatory element that can activate a gene from a distance.
Later researchers have found similar results—that TEs can influence gene transcription—in other
species, such as fruit flies, morning glory flowers, and (vindicating McClintock's suspicions) maize
(Slotkin & Martienssen, 2007). Moreover, in primates, scientists have identified a SINE known as Alu
that seems to play an important role in gene regulation and evolution. These new discoveries are
prompting scientists to think twice about dismissing such a large portion of the genome as nothing but
"junk."
References and Recommended Reading
Bejerano, G., et al. A distal enhancer and an ultra conserved exon are derived from a novel
retrotransposon. Nature 441, 87–90 (2006) doi:10.1038/nature04696 (link to articles)
Britten, R. J., & Davidson, E. H. Gene regulation for higher cells: A theory. Science 165, 349–357
(1969)
McClintock, B. Components of action of the regulators Spm and Ac. Carnegie Institution of
Washington Year Book 64, 527–536 (1965)
Ogiwara, I., et al. V-SINEs: A new superfamily of vertebrate SINEs that are widespread in vertebrate
genomes and retain a strongly conserved segment within each repetitive unit. Genome Research 12,
316–324 (2002)
Pennisi, E. Jumping genes hop into the evolutionary limelight. Science 317, 894–895 (2007)
Slotkin, R. K., & Martienssen, R. Transposable elements and the epigenetic regulation of the genome.
Nature Reviews Genetics 8, 272–285 (2007) doi:10.1038/nrg2072 (link to articles)
Smit, A. F. A. Interspersed repeats and other mementos of transposable elements in mammalian
genomes. Current Opinion in Genetics and Development 9, 657–663 (1999)
Source: http://www.nature.com/scitable/topicpage/transposons-or-jumping-genes-not-junk-dna-1211#