transposon (jumping gene, transposable element, mobile genetic element, selfish DNA)
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Introduction
Sequence of mobile DNA able to move to different positions within the genome of a single cell (transposition).
In the process of transposition, they may cause mutations &/or change the amount of DNA in the genome.
Found in all major branches of life.
Classification
May be grouped based on their mechanism of transposition:
- retrotransposons (class 1)
- class 2 transposons (DNA transposons)
The most common form of transposon in humans is the Alu sequence
Pathology
- transposons are mutagens
- they can damage the genome of their host cell:
- a transposon or a retroposon that inserts itself into a functional gene will most likely disable that gene
- after a transposon leaves a gene, the resulting gap will probably not be repaired correctly
- multiple copies of the same sequence, such as Alu sequences can hinder precise chromosomal pairing during mitosis, resulting in unequal crossovers, one of the main reasons for chromosome duplication
- diseases often caused by transposons include:
- transposons may predispose to cancer
- many transposons contain promoters which drive transcription of their own transposase; these promoters can cause aberrant expression of linked genes, causing disease or mutant phenotypes
Mechanisms adapted for reducing transposon activity include:
Transposons are used as a research tool to alter DNA inside a living organism. Transposons make up a large fraction of genome sizes of eukaryotic species (40% of human DNA)[3]
Physiology
- may have provided a means of producing antibody diversity
- V(D)J recombination system operates by a mechanism similar to that of transposons
- evolution of autosomal retrogenes from X-linked progenitors compensates for X-chromosome silencing during male meiosis
More general terms
More specific terms
Additional terms
References
- ↑ Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Transposon
- ↑ McClintock, B. The origin and behavior of mutable loci in maize. Proc Natl Acad Sci U S A. (1950) 36(6): 344-55. PMID: https://www.ncbi.nlm.nih.gov/pubmed/15430309
- ↑ 3.0 3.1 Grandi N, Tramontano E. Human Endogenous Retroviruses Are Ancient Acquired Elements Still Shaping Innate Immune Responses. Frontiers in Immunology, 2018. Sept 10 PMID: https://www.ncbi.nlm.nih.gov/pubmed/30250470 PMCID: PMC6139349 Free PMC article