Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-4-13
pubmed:abstractText
DNA end-joining was measured by incubating linearized plasmid DNA with mitochondrial protein extracts. A spectrum of end-joined molecules ranging from re-circularized monomer to dimer and higher molecular weight forms was observed. The DNA end-joining reaction required ATP and Mg2+, and was inhibited by sodium chloride. Both cohesive- and blunt-ended DNA molecules were end-joined, although the former were more efficient substrates. Molecular analysis of rejoined molecules revealed that >95% of the linearized DNA were precisely end-joined. The few imprecisely end-joined molecules recovered, sustained deletions that spanned direct repeat sequences. The deletions observed are strikingly similar to those present in mitochondrial genomes of patients with Kearns-Sayre or Pearson syndromes, certain ophthalmic myopathies and the aged. These results suggest that mammalian mitochondria possess a DNA double strand break repair activity similar to that seen in the nucleus, and that this repair pathway may play a role in the generation of mitochondrial DNA deletions associated with a number of human pathologies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0305-1048
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1198-204
pubmed:dateRevised
2008-11-20
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Double strand break rejoining by mammalian mitochondrial extracts.
pubmed:affiliation
Department of Pharmacology, University of Minnesota Medical School, 3-249 Millard Hall, Minneapolis, MN 55455, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't