✍ Scribed by Arturas Petronis
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Evidence for recombination suppression has been identified in linkage studies of several unstable DNA diseases. Also sex-specific changes in recombination frequency have been detected at the loci of Huntington's disease and myotonic dystrophy. It can be hypothesized that meiotic recombination is regulated by genome-wide genomic imprinting and that changes in meiotic recombination imply the presence of the genomic imprinting defect. If aberrant recombination at the locus of trinucleotide repeat expansion is verified, new theoretical and experimental opportunities will arise in studies on the role of genomic imprinting Accepted
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Background. Deletion of the distal short arm of chromosome 1 occurs in 25-35% of primary neuroblastomas, and a putative tumor suppressor gene has been mapped to a consensus region of deletion at 1p36.2-36.3. Indirect evidence suggests the presence of an imprinted neuroblastoma suppressor gene within