Editing Transposable element (section)

== Evolution ==

TEs are found in almost all life forms, and the scientific community is still exploring their evolution and their effect on genome evolution. It is unclear whether TEs originated in the [[last universal common ancestor]], arose independently multiple times, or arose once and then spread to other kingdoms by [[horizontal gene transfer]].<ref>{{cite journal | vauthors = Kidwell MG | s2cid = 33227644 | title = Horizontal transfer of P elements and other short inverted repeat transposons | journal = Genetica | volume = 86 | issue = 1–3 | pages = 275–86 | year = 1992 | pmid = 1334912 | doi = 10.1007/BF00133726 }}</ref>

Because excessive TE activity can damage [[exon]]s, many organisms have acquired mechanisms to inhibit their activity. Bacteria may undergo high rates of [[gene deletion]] as part of a mechanism to remove TEs and viruses from their genomes, while [[Eukaryote|eukaryotic]] organisms typically use [[RNA interference]] to inhibit TE activity. Nevertheless, some TEs generate large families often associated with [[speciation]] events.<ref>{{cite journal |last1=Ricci |first1=Marco |last2=Peona |first2=Valentina |last3=Guichard |first3=Etienne |last4=Taccioli |first4=Cristian |last5=Boattini |first5=Alessio |title=Transposable Elements Activity is Positively Related to Rate of Speciation in Mammals |journal=Journal of Molecular Evolution |date=31 May 2018 |volume=86 |issue=5 |pages=303–310 |doi=10.1007/s00239-018-9847-7 |pmid=29855654 |pmc=6028844 |bibcode=2018JMolE..86..303R }}</ref> Evolution often deactivates DNA transposons, leaving them as [[intron]]s (inactive gene sequences). In vertebrate animal cells, nearly all 100,000+ DNA transposons per genome have genes that encode inactive transposase polypeptides.<ref>{{cite journal | vauthors = Plasterk RH, Izsvák Z, Ivics Z | title = Resident aliens: the Tc1/mariner superfamily of transposable elements | journal = Trends in Genetics | volume = 15 | issue = 8 | pages = 326–32 | date = August 1999 | pmid = 10431195 | doi = 10.1016/S0168-9525(99)01777-1 }}</ref> The first synthetic transposon designed for use in vertebrate (including human) cells, the [[Sleeping Beauty transposon system]], is a Tc1/mariner-like transposon. Its dead ("fossil") versions are spread widely in the salmonid genome and a functional version was engineered by comparing those versions.<ref>{{cite journal | vauthors = Ivics Z, Hackett PB, Plasterk RH, Izsvák Z | s2cid = 17908472 | title = Molecular reconstruction of Sleeping Beauty, a Tc1-like transposon from fish, and its transposition in human cells | journal = Cell | volume = 91 | issue = 4 | pages = 501–10 | date = November 1997 | pmid = 9390559 | doi = 10.1016/S0092-8674(00)80436-5 | doi-access = free }}</ref> Human Tc1-like transposons are divided into Hsmar1 and Hsmar2 subfamilies. Although both types are inactive, one copy of Hsmar1 found in the [[SETMAR]] gene is under selection as it provides DNA-binding for the histone-modifying protein.<ref>{{cite journal | vauthors = Miskey C, Papp B, Mátés L, Sinzelle L, Keller H, Izsvák Z, Ivics Z | title = The ancient mariner sails again: transposition of the human Hsmar1 element by a reconstructed transposase and activities of the SETMAR protein on transposon ends | journal = Molecular and Cellular Biology | volume = 27 | issue = 12 | pages = 4589–600 | date = June 2007 | pmid = 17403897 | pmc = 1900042 | doi = 10.1128/MCB.02027-06 }}</ref> Many other human genes are similarly derived from transposons.<ref>{{cite web |title=Gene group: Transposable element derived genes |url=https://www.genenames.org/data/genegroup/#!/group/1416 |publisher=HUGO Gene Nomenclature Committee |access-date=4 March 2019}}</ref> Hsmar2 has been reconstructed multiple times from the fossil sequences.<ref>{{cite journal | vauthors = Gil E, Bosch A, Lampe D, Lizcano JM, Perales JC, Danos O, Chillon M | title = Functional characterization of the human mariner transposon Hsmar2 | journal = PLOS ONE| volume = 8 | issue = 9 | pages = e73227 | date = 11 September 2013 | pmid = 24039890 | pmc = 3770610 | doi = 10.1371/journal.pone.0073227 | bibcode = 2013PLoSO...873227G | doi-access = free }}</ref>

The frequency and location of TE integrations influence genomic structure and evolution and affect gene and protein regulatory networks during development and in differentiated cell types.<ref>{{Cite journal |last1=Ball |first1=Hope C. |last2=Ansari |first2=Mohammad Y. |last3=Ahmad |first3=Nashrah |last4=Novak |first4=Kimberly |last5=Haqqi |first5=Tariq M. |date=November 2021 |title=A retrotransposon gag-like-3 gene RTL3 and SOX-9 co-regulate the expression of COL2A1 in chondrocytes |journal=Connective Tissue Research |volume=62 |issue=6 |pages=615–628 |doi=10.1080/03008207.2020.1828380 |issn=1607-8438 |pmc=8404968 |pmid=33043724}}</ref> Large quantities of TEs within genomes may still present evolutionary advantages, however. [[Interspersed repeat]]s within genomes are created by transposition events accumulating over evolutionary time. Because interspersed repeats block [[gene conversion]], they protect novel gene sequences from being overwritten by similar gene sequences and thereby facilitate the development of new genes. TEs may also have been co-opted by the [[Adaptive immune system|vertebrate immune system]] as a means of producing antibody diversity. The [[V(D)J recombination]] system operates by a mechanism similar to that of some TEs. TEs also serve to generate repeating sequences that can form [[dsRNA]] to act as a substrate for the action of [[ADAR]] in RNA editing.<ref>{{cite journal | vauthors = Jin Y, Zhang W, Li Q | title = Origins and evolution of ADAR-mediated RNA editing | journal = IUBMB Life| volume = 61 | issue = 6 | pages = 572–578 | date = June 2009 | doi = 10.1002/iub.207| pmid = 19472181 | doi-access = free }}</ref>

TEs can contain many types of genes, including those conferring antibiotic resistance and the ability to transpose to conjugative plasmids. Some TEs also contain [[integron]]s, genetic elements that can capture and express genes from other sources. These contain [[integrase]], which can integrate [[gene cassette]]s. There are over 40 antibiotic resistance genes identified on cassettes, as well as virulence genes.

Transposons do not always excise their elements precisely, sometimes removing the adjacent base pairs; this phenomenon is called [[exon shuffling]]. Shuffling two unrelated exons can create a novel gene product or, more likely, an intron.<ref>{{cite journal | vauthors = Moran JV, DeBerardinis RJ, Kazazian HH | title = Exon shuffling by L1 retrotransposition | journal = Science | volume = 283 | issue = 5407 | pages = 1530–4 | date = March 1999 | pmid = 10066175 | doi = 10.1126/science.283.5407.1530 | bibcode = 1999Sci...283.1530M }}</ref>

Some non-autonomous DNA TEs found in plants can capture coding DNA from genes and shuffle them across the genome.<ref>{{cite journal | vauthors = Jiang N, Bao Z, Zhang X, Eddy SR, Wessler SR | title = Pack-MULE transposable elements mediate gene evolution in plants | journal = Nature | volume = 431 | issue = 7008 | pages = 569–573 | date = September 2004 | pmid = 15457261 | doi = 10.1038/nature02953 | bibcode = 2004Natur.431..569J | s2cid = 4363679 }}</ref> This process can duplicate genes in the genome (a phenomenon called transduplication), and can contribute to generate novel genes by exon shuffling.<ref>{{cite journal | vauthors = Catoni M, Jonesman T, Cerruti E, Paszkowski J | title = Mobilization of Pack-CACTA transposons in Arabidopsis suggests the mechanism of gene shuffling | journal = Nucleic Acids Research | volume = 47 | issue = 3 | pages = 1311–1320 | date = February 2019 | pmid = 30476196 | pmc = 6379663 | doi = 10.1093/nar/gky1196 }}</ref>

=== Evolutionary drive for TEs on the genomic context ===
There is a hypothesis that states that TEs might provide a ready source of DNA that could be co-opted by the cell to help regulate gene expression. Research showed that many diverse modes of TEs co-evolution along with some transcription factors targeting TE-associated genomic elements and chromatin are evolving from TE sequences. Most of the time, these particular modes do not follow the simple model of TEs and regulating host gene expression.<ref name="Zhou 19359–19366"/>