Breakpoints of gross deletions coincide with non-B DNA conformations
AUTOR(ES)
Bacolla, Albino
FONTE
National Academy of Sciences
RESUMO
Genomic rearrangements are a frequent source of instability, but the mechanisms involved are poorly understood. A 2.5-kbp poly(purine·pyrimidine) sequence from the human PKD1 gene, known to form non-B DNA structures, induced long deletions and other instabilities in plasmids that were mediated by mismatch repair and, in some cases, transcription. The breakpoints occurred at predicted non-B DNA structures. Distance measurements also indicated a significant proximity of alternating purine-pyrimidine and oligo(purine·pyrimidine) tracts to breakpoint junctions in 222 gross deletions and translocations, respectively, involved in human diseases. In 11 deletions analyzed, breakpoints were explicable by non-B DNA structure formation. We conclude that alternative DNA conformations trigger genomic rearrangements through recombination-repair activities.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=521098Documentos Relacionados
- Non-A, Non-B Hepatitis
- A cDNA clone closely associated with non-A, non-B hepatitis.
- Yeast regulatory sequences preferentially adopt a non-B conformation in supercoiled DNA.
- Chronic non-A, non-B hepatitis: role of hepatitis C virus.
- Detection of non-A, non-B hepatitis antigen by immunocytochemical staining.