a microhomology-mediated break-induced replication model for the origin of human copy number variation一个microhomology-mediated断路感应复制模型的起源人类拷贝数变异.pdfVIP

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a microhomology-mediated break-induced replication model for the origin of human copy number variation一个microhomology-mediated断路感应复制模型的起源人类拷贝数变异.pdf

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a microhomology-mediated break-induced replication model for the origin of human copy number variation一个microhomology-mediated断路感应复制模型的起源人类拷贝数变异

Review A Microhomology-Mediated Break-Induced Replication Model for the Origin of Human Copy Number Variation 1 1 1,2,3 P. J. Hastings *, Grzegorz Ira , James R. Lupski 1 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America, 2 Department of Pediatrics, Baylor College of Medicine, Houston, Texas, United States of America, 3 Texas Children’s Hospital, Houston, Texas, United States of America recombination between segments that already occur as two or Abstract: Chromosome structural changes with nonre- more copies. When this happens, sequences that lie between the current endpoints associated with genomic disorders repeats that recombine will be either duplicated or deleted, thus offer windows into the mechanism of origin of copy changing the copy number. This process is referred to as nonallelic number variation (CNV). A recent report of nonrecurrent homologous recombination, or NAHR [18]. The repeated duplications associated with Pelizaeus-Merzbacher dis- sequences that recombine might occasionally be highly repetitive ease identified three distinctive characteristics. First, the sequences that occur widely in the human genome [19] but are majority of events can be seen to be complex, showing discontinuous duplications mixed with deletions, inverted usually sequences that occur only twi