TEs are mutagens 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.
TEs can damage the genome of their host cell in different ways:
* 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 sequences, can hinder precise chromosomal pairing during mitosis and meiosis, resulting in unequal 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 promoters which drive transcription of their own transposase. These promoters can cause aberrant expression of linked genes, causing disease or mutant phenotypes.