Editing Genome (section)

==== Tandem repeats ====
Short, non-coding sequences that are repeated head-to-tail are called [[tandem repeats]]. Microsatellites consisting of 2–5 basepair repeats, while minisatellite repeats are 30–35 bp. Tandem repeats make up about 4% of the human genome and 9% of the fruit fly genome.<ref name="Padeken">{{cite journal |vauthors = Padeken J, Zeller P, Gasser SM |title = Repeat DNA in genome organization and stability |journal = Current Opinion in Genetics & Development |volume = 31 |pages = 12–19 |date = April 2015 |pmid = 25917896 |doi = 10.1016/j.gde.2015.03.009 }}</ref> Tandem repeats can be functional. For example, [[telomere]]s are composed of the tandem repeat TTAGGG in mammals, and they play an important role in protecting the ends of the chromosome.

In other cases, expansions in the number of tandem repeats in exons or introns can cause [[Trinucleotide repeat disorder|disease]].<ref name="Usdin">{{cite journal |vauthors = Usdin K |title = The biological effects of simple tandem repeats: lessons from the repeat expansion diseases |journal = Genome Research |volume = 18 |issue = 7 |pages = 1011–19 |date = July 2008 |pmid = 18593815 |pmc = 3960014 |doi = 10.1101/gr.070409.107 }}</ref> For example, the human gene huntingtin (Htt) typically contains 6–29 tandem repeats of the nucleotides CAG (encoding a polyglutamine tract). An expansion to over 36 repeats results in [[Huntington's disease]], a neurodegenerative disease. Twenty human disorders are known to result from similar tandem repeat expansions in various genes. The mechanism by which proteins with expanded polygulatamine tracts cause death of neurons is not fully understood. One possibility is that the proteins fail to fold properly and avoid degradation, instead accumulating in aggregates that also sequester important transcription factors, thereby altering gene expression.<ref name="Usdin"/>

Tandem repeats are usually caused by slippage during replication, unequal crossing-over and gene conversion.<ref>{{cite journal |vauthors = Li YC, Korol AB, Fahima T, Beiles A, Nevo E |title = Microsatellites: genomic distribution, putative functions and mutational mechanisms: a review |journal = Molecular Ecology |volume = 11 |issue = 12 |pages = 2453–65 |date = December 2002 |pmid = 12453231 |doi = 10.1046/j.1365-294X.2002.01643.x |s2cid = 23606208 |doi-access = free |bibcode = 2002MolEc..11.2453L }}</ref>