Source:http://linkedlifedata.com/resource/pubmed/id/15467361
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-4
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pubmed:dateCreated |
2004-10-6
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pubmed:abstractText |
In Drosophila females, the majority of recombination events do not become crossovers and those that do occur are nonrandomly distributed. Furthermore, a group of Drosophila mutants specifically reduce crossing over, suggesting that crossovers depend on different gene products than noncrossovers. In mei-218 mutants, crossing over is reduced by approximately 90% while noncrossovers and the initiation of recombination remain unchanged. Importantly, the residual crossovers have a more random distribution than wild-type. It has been proposed that mei-218 has a role in establishing the crossover distribution by determining which recombination sites become crossovers. Surprisingly, a diverse group of genes, including those required for double strand break (DSB) formation or repair, have an effect on crossover distribution. Not all of these mutants, however, have a crossover-specific defect like mei-218 and it is not understood why some crossover-defective mutants alter the distribution of crossovers. Intragenic recombination experiments suggest that mei-218 is required for a molecular transition of the recombination intermediate late in the DSB repair pathway. We propose that the changes in crossover distribution in some crossover-defective mutants are a secondary consequence of the crossover reductions. This may be the activation of a regulatory system that ensures at least one crossover per chromosome, and which compensates for an absence of crossovers by attempting to generate them at random locations.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1424-859X
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2004 S. Karger AG, Basel.
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pubmed:issnType |
Electronic
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pubmed:volume |
107
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
160-71
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15467361-Alleles,
pubmed-meshheading:15467361-Animals,
pubmed-meshheading:15467361-Cell Cycle Proteins,
pubmed-meshheading:15467361-Crossing Over, Genetic,
pubmed-meshheading:15467361-DNA Damage,
pubmed-meshheading:15467361-DNA Repair,
pubmed-meshheading:15467361-Drosophila Proteins,
pubmed-meshheading:15467361-Drosophila melanogaster,
pubmed-meshheading:15467361-Female,
pubmed-meshheading:15467361-Genotype,
pubmed-meshheading:15467361-Male,
pubmed-meshheading:15467361-Meiosis,
pubmed-meshheading:15467361-Mutation,
pubmed-meshheading:15467361-Synaptonemal Complex,
pubmed-meshheading:15467361-X-Rays
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pubmed:year |
2004
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pubmed:articleTitle |
Studies on crossover-specific mutants and the distribution of crossing over in Drosophila females.
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pubmed:affiliation |
Waksman Institute and Department of Genetics, Rutgers, the State University of New Jersey, Piscataway, NJ 08854, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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