Admin: 1 версия импортирована

2025-11-13T18:01:10Z

1 версия импортирована

← Предыдущая версия		Версия от 18:01, 13 ноября 2025
(нет различий)

ru>InternetArchiveBot: Rescuing 0 sources and tagging 1 as dead.) #IABot (v2.0.9.5) (Eastmain - 17917

2024-03-09T20:22:03Z

Rescuing 0 sources and tagging 1 as dead.) #IABot (v2.0.9.5) (Eastmain - 17917

Новая страница

'''Non-allelic homologous recombination''' ('''NAHR''') is a form of [[homologous recombination]] that occurs between two lengths of [[DNA]] that have high sequence similarity, but are not [[allele]]s.<ref name=Hurles/><ref name="pmid17637735">{{cite journal |vauthors=Beckmann JS, Estivill X, Antonarakis SE |title=Copy number variants and genetic traits: closer to the resolution of phenotypic to genotypic variability |journal=Nat. Rev. Genet. |volume=8 |issue=8 |pages=639–46 |date=August 2007 |pmid=17637735 |doi=10.1038/nrg2149 |s2cid=32906877 }}</ref><ref>{{Cite journal|title = The consequences of structural genomic alterations in humans: Genomic Disorders, genomic instability and cancer|last = Colnaghi|first = Rita|date = July 2011|journal = Seminars in Cell & Developmental Biology|doi = 10.1016/j.semcdb.2011.07.010|pmid = 21802523|volume=22|issue = 8|pages=875–885}}</ref>

It usually occurs between sequences of DNA that have been previously [[Segmental duplication|duplicated]] through evolution, and therefore have [[low copy repeats]] (LCRs). These repeat elements typically range from 10–300 kb in length and share 95-97% sequence identity.<ref name=":0">{{Cite journal|title = The consequences of structural genomic alterations in humans: Genomic Disorders, genomic instability and cancer|journal = Seminars in Cell & Developmental Biology|date = 2011-10-01|pages = 875–885|volume = 22|series = Polarized growth and movement: How to generate new shapes and structuresChromosome Recombination|issue = 8|doi = 10.1016/j.semcdb.2011.07.010|pmid = 21802523|first1 = Rita|last1 = Colnaghi|first2 = Gillian|last2 = Carpenter|first3 = Marcel|last3 = Volker|first4 = Mark|last4 = O’Driscoll}}</ref> During [[meiosis]], LCRs can misalign and subsequent [[Chromosomal crossover|crossing-over]] can result in genetic rearrangement.<ref name=":0" /> When non-allelic homologous recombination occurs between different LCRs, [[Deletion (genetics)|deletions]] or further [[Gene duplication|duplications]] of the DNA can occur. This can give rise to rare [[genetic disorder]]s, caused by the loss or increased copy number of genes within the deleted or duplicated region. It can also contribute to the [[copy number variation]] seen in some gene clusters.<ref name="pmid20333217">{{cite journal |vauthors=Karn RC, Laukaitis CM |title=The mechanism of expansion and the volatility it created in three pheromone gene clusters in the mouse (Mus musculus) genome |journal=Genome Biol Evol |volume=1 |pages=494–503 |year=2009 |pmid=20333217 |pmc=2839280 |doi=10.1093/gbe/evp049 }}</ref>

As LCRs are often found in "hotspots" in the human genome, some [[chromosomal]] regions are particularly prone to NAHR.<ref name=Hurles>{{Citation
|last = Hurles
|first = Matthew
|contribution = Recombination Hotspots in Nonallelic Homologous Recombination
|title = Genomic Disorders: The Genomic Basis of Disease
|pages = 341–355
|publisher = Humana Press
|year = 2006
|contribution-url = http://www.springerlink.com/content/um222230u28p1719/
|display-authors = etal
}}{{Dead link|date=March 2024 |bot=InternetArchiveBot |fix-attempted=yes }}</ref> Recurrent rearrangements are nucleotide sequence variations found in multiple individuals, sharing a common size and location of break points.<ref name=":0" /> Therefore, multiple patients may manifest with similar deletions or duplications, resulting in the description of genetic [[syndrome]]s. Examples of these include [[Neurofibromatosis type I|NF1 microdeletion syndrome]], [[17q21.3 recurrent microdeletion syndrome]] or [[3q29 microdeletion syndrome]].<ref name="pmid15103551">{{cite journal |vauthors=Venturin M, Gervasini C, Orzan F, etal |title=Evidence for non-homologous end joining and non-allelic homologous recombination in atypical NF1 microdeletions |journal=Hum. Genet. |volume=115 |issue=1 |pages=69–80 |date=June 2004 |pmid=15103551 |doi=10.1007/s00439-004-1101-2 |s2cid=22263143 }}</ref><ref name="pmid18628315">{{cite journal |vauthors=Koolen DA, Sharp AJ, Hurst JA, etal |title=Clinical and molecular delineation of the 17q21.31 microdeletion syndrome |journal=J. Med. Genet. |volume=45 |issue=11 |pages=710–20 |date=November 2008 |pmid=18628315 |doi=10.1136/jmg.2008.058701 |pmc=3071570}}</ref><ref name="pmid15918153">{{cite journal |vauthors=Willatt L, Cox J, Barber J, etal |title=3q29 microdeletion syndrome: clinical and molecular characterization of a new syndrome |journal=Am. J. Hum. Genet. |volume=77 |issue=1 |pages=154–60 |date=July 2005 |pmid=15918153 |pmc=1226188 |doi=10.1086/431653 }}</ref>

==See also==
* [[Genetic recombination]]
* [[Non-homologous end joining]]

==References==
{{Reflist}}

{{DEFAULTSORT:Non-allelic homologous recombination}}
[[Category:Genetics]]

{{genetics-stub}}

Non-allelic homologous recombination - История изменений

Admin: 1 версия импортирована

ru>InternetArchiveBot: Rescuing 0 sources and tagging 1 as dead.) #IABot (v2.0.9.5) (Eastmain - 17917