Editing Transposable element (section)

=== Mechanisms of mutagenesis ===
TEs are [[mutagen]]s and due to the contribution to the formation of new cis-regulatory DNA elements that are connected to many transcription factors that are found in living cells; TEs can undergo many evolutionary mutations and alterations. These are often the causes of genetic disease, and gives the potential lethal effects of ectopic expression.<ref name="Zhou 19359–19366"/>

TEs can damage the genome of their host cell in different ways:<ref name=":0" />

* A transposon or a retrotransposon that inserts itself into a functional gene can disable that gene.
* After a DNA transposon leaves a gene, the resulting gap may not be repaired correctly.
* Multiple copies of the same sequence, such as [[Alu sequence]]s, can hinder precise [[Chromosome|chromosomal]] pairing during [[mitosis]] and [[meiosis]], resulting in unequal [[Chromosomal crossover|crossovers]], one of the main reasons for chromosome duplication.

TEs use a number of different mechanisms to cause genetic instability and disease in their host genomes.

* Expression of disease-causing, damaging proteins that inhibit normal cellular function.
** Many TEs contain [[Promoter (genetics)|promoters]] which drive [[Transcription (genetics)|transcription]] of their own [[transposase]]. These promoters can cause aberrant expression of linked genes, causing disease or [[mutant]] [[phenotypes]].<ref>{{cite journal | vauthors = Dahlet T, Argüeso Lleida A, Al Adhami H, Dumas M, Bender A, Ngondo RP, Tanguy M, Vallet J, Auclair G, Bardet AF, Weber M | display-authors = 6 | title = Genome-wide analysis in the mouse embryo reveals the importance of DNA methylation for transcription integrity | journal = Nature Communications | volume = 11 | issue = 1 | pages = 3153 | date = June 2020 | pmid = 32561758 | pmc = 7305168 | doi = 10.1038/s41467-020-16919-w | bibcode = 2020NatCo..11.3153D }}</ref>