HistoryThis section has been translated automatically.
In 1983, the US botanist Barbara McClintock was awarded the Nobel Prize for the discovery of the transposon (McClintock B 1950).
DefinitionThis section has been translated automatically.
A transposon is a so-called parasitic DNA (genetic snippet) that occurs in prokaryotes and eukaryotes. They make up about 3% of the human genome. They are short DNA segments in the genome which, with the help of enzymes such as transposase and resolvase, repeatedly copy themselves and are then incorporated into the genome at new sites (transposition).
Transposition always occurs via so-called "illegitimate recombination", i.e. there is no homology whatsoever between the sequence at the integration site in the genome and that of the T. Transposons are thus able to induce more complex changes in the genome and possibly even cause recombinations of functional gene regions, as is conceivable, for example, by relocation and recombination of exons.
Transposons are a major cause of spontaneously occurring mutations. In addition to gene mutations, their integration also leads to chromosomal mutations that manifest themselves at the molecular level as breaks, deletions, or inversions. Estimates for prokaryotes showed that up to 40 % of all mutations are due to the action of mobile genetic elements.
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ClassificationThis section has been translated automatically.
A distinction is made between:
- RNA transposons whose mobile intermediate is formed by RNA (retroelements/retrotransposons or class I transposon)
- DNA transposons or class II transposons (Babakhani S et al. 2018).
For the latter, a distinction is made between conservative transposition and replicative transposition. While in conservative transposition the transposon is cut out of the DNA and reinserted elsewhere ("cut & paste"), in replicative transposition the transposon is not cut out but a copy is made which is inserted elsewhere ("copy & paste"). In replicative transposition, the number of transposons is increased. The transposon is cut out or copied with the help of the enzyme transposase. DNA transposons that are too small to code for a protein are calledminiature inverted-repeat transposable elements(MITEs). They cannot propagate autonomously. How they propagate or translocate is still unclear. It is possible that the transposase gene was once present and is now defective or lost. It is possible that MITEs copy and move through transposase enzymes encoded by other, larger transposons that have the same recognition sequence (inverted repeats).
RNA transposons jump by being transcribed into mRNA, which is subsequently transcribed into cDNA (by a reverse transcriptase) and reintegrated. In the process, the retroelements proliferate. The subclass of so-called SINEs, but also other retroelements that are no longer autonomous, no longer have a reverse transcriptase and are dependent on a foreign transcriptase (for example from other retroelements).
General informationThis section has been translated automatically.
The enzymes involved, transposases, recognize the ends of the transposons and lead to single-strand breaks there and at the integration site of the DNA strand. The insertion of a transposon generates a short duplication at the integration site, which comprises a different number of base pairs depending on the transposon. Transposons that jump into the coding region of a gene usually lead to its inactivation. If, on the other hand, integration occurs in the promoter or other regulatory elements, gene expression can either be switched on or off, depending on the T. species.
Control mechanisms: A variety of molecular mechanisms exist in a cell that are involved in the control of such transposons and prevent their propagation. One of these mechanisms, which specifically protects germline cells, relies on certain Argonaute class proteins called Piwi proteins and small RNA molecules bound to these proteins called piRNAs. Piwi proteins can specifically deactivate transposons because their piRNAs recognise the transposons according to the lock-and-key principle, dock onto them and shut them down.
Note(s)This section has been translated automatically.
The effects of transposition are profound, as more than 100 human genetic diseases can be attributed to transposon insertions (Kumar A 2020). Transposition can be highly mutagenic and disrupt genome integrity and gene expression in a variety of organisms. For example, transposons from bacteria usually contain genes that mediate antibiotic resistance. Transposons can transfer from one plasmid to other plasmids or from a DNA chromosome to a plasmid and vice versa, resulting in the transfer of antibiotic resistance genes in bacteria. Bacterial transposons of this type belong to the Tn family. Thus, Acinetobacter species evolved into important nosocomial pathogens due to their broad antibiotic resistance. A key factor for these multi-drug resistance phenotypes is the acquisition of a variety of mobile genetic elements, especially large conjugative plasmids. The plasmid family has a highly dynamic and diverse accessory genome containing 221 antibiotic resistance genes (ARGs) conferring resistance to 13 classes of antibiotics (Ghaly TM et al. 2020).
LiteratureThis section has been translated automatically.
- Babakhani S et al. (2018) Transposons: the agents of antibiotic resistance in bacteria. J Basic Microbiol 58:905-917.
- Frost LS et al (2005) Mobile genetic elements: the agents of open source evolution. Nat Rev Microbiol 3:722-32
- Ghaly TM et al (2020) A Novel Family of Acinetobacter Mega-Plasmids Are Disseminating Multi-Drug Resistance Across the Globe While Acquiring Location-Specific Accessory Genes. Front Microbiol 11:605952.
- Kumar A (2020) Jump around: transposons in and out of the laboratory. F1000Res 24: F1000 Faculty Rev-135.
- McClintock B (1950): The origin and behavior of mutable loci in maize. In: Proceedings of the National Academy of Sciences 36: 344-355.
- Raiz J et al. (2012): The non-autonomous retrotransposon SVA is trans-mobilized by the human LINE-1 protein machinery.Nucleic Acids Res 40: 1666-1683.