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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
16
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pubmed:dateCreated |
1991-9-18
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pubmed:abstractText |
The nod (no distributive disjunction) and the ncd (non-claret disjunctional) mutations are both female-specific, recessive meiotic mutations in Drosophila melanogaster. Mutations at either locus show high frequencies of nondisjunction at meiosis I and both have been shown to encode kinesin-like proteins. Unlike the ncd mutation, which affects all chromosome pairs, the nod mutation affects only the disjunction of nonexchange chromosomes. Although both the nod and ncd mutations are fully recessive, females doubly heterozygous for nod and ncd mutations show levels of X and fourth chromosome nondisjunction that are 6- to 35-fold above those observed in control females. Exchange between chromosomes can suppress this effect; thus, only nonexchange chromosomes segregating via the distributive system are sensitive in double heterozygotes. Since the phenotype of double heterozygotes mimics that of the nod mutation, we infer that ncd is a dominant enhancer of nod. Failure of ncd to fully complement nod reveals the chromosome segregation machinery to be dosage sensitive. The probability that the distributive system will fail is enhanced in females simultaneously haploinsufficient at the nod and ncd loci.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-13950302,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-1691829,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-17248428,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2111262,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2140958,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2144792,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2146510,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2261638,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2479546,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2498648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2503421,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-2513253,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-4442702,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-4633612,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-5339860,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1908090-6413518
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
88
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pubmed:geneSymbol |
ncd,
nod
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7165-9
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pubmed:dateRevised |
2010-9-10
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pubmed:meshHeading |
pubmed-meshheading:1908090-Animals,
pubmed-meshheading:1908090-Chromosome Mapping,
pubmed-meshheading:1908090-Crosses, Genetic,
pubmed-meshheading:1908090-Drosophila melanogaster,
pubmed-meshheading:1908090-Enhancer Elements, Genetic,
pubmed-meshheading:1908090-Female,
pubmed-meshheading:1908090-Genes, Dominant,
pubmed-meshheading:1908090-Genes, Recessive,
pubmed-meshheading:1908090-Genetic Complementation Test,
pubmed-meshheading:1908090-Genotype,
pubmed-meshheading:1908090-Homozygote,
pubmed-meshheading:1908090-Male,
pubmed-meshheading:1908090-Microtubule Proteins,
pubmed-meshheading:1908090-Mitosis,
pubmed-meshheading:1908090-Mutation,
pubmed-meshheading:1908090-Nondisjunction, Genetic,
pubmed-meshheading:1908090-X Chromosome,
pubmed-meshheading:1908090-Y Chromosome
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pubmed:year |
1991
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pubmed:articleTitle |
Genetic analysis of microtubule motor proteins in Drosophila: a mutation at the ncd locus is a dominant enhancer of nod.
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pubmed:affiliation |
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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