| pubmed-article:1732169 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1732169 | lifeskim:mentions | umls-concept:C0043393 | lld:lifeskim |
| pubmed-article:1732169 | lifeskim:mentions | umls-concept:C0039062 | lld:lifeskim |
| pubmed-article:1732169 | lifeskim:mentions | umls-concept:C0008633 | lld:lifeskim |
| pubmed-article:1732169 | lifeskim:mentions | umls-concept:C0598501 | lld:lifeskim |
| pubmed-article:1732169 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:1732169 | lifeskim:mentions | umls-concept:C1155792 | lld:lifeskim |
| pubmed-article:1732169 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1732169 | pubmed:dateCreated | 1992-2-25 | lld:pubmed |
| pubmed-article:1732169 | pubmed:abstractText | A mutation at the REC102 locus was identified in a screen for yeast mutants that produce inviable spores. rec102 spore lethality is rescued by a spo13 mutation, which causes cells to bypass the meiosis I division. The rec102 mutation completely eliminates meiotically induced gene conversion and crossing over but has no effect on mitotic recombination frequencies. Cytological studies indicate that the rec102 mutant makes axial elements (precursors to the synaptonemal complex), but homologous chromosomes fail to synapse. In addition, meiotic chromosome segregation is significantly delayed in rec102 strains. Studies of double and triple mutants indicate that the REC102 protein acts before the RAD52 gene product in the meiotic recombination pathway. The REC102 gene was cloned based on complementation of the mutant defect and the gene was mapped to chromosome XII between CDC25 and STE11. | lld:pubmed |
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| pubmed-article:1732169 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1732169 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1732169 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1732169 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1732169 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:1732169 | pubmed:issn | 0016-6731 | lld:pubmed |
| pubmed-article:1732169 | pubmed:author | pubmed-author:RoederG SGS | lld:pubmed |
| pubmed-article:1732169 | pubmed:author | pubmed-author:EngebrechtJJ | lld:pubmed |
| pubmed-article:1732169 | pubmed:author | pubmed-author:BhargavaJJ | lld:pubmed |
| pubmed-article:1732169 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1732169 | pubmed:volume | 130 | lld:pubmed |
| pubmed-article:1732169 | pubmed:geneSymbol | REC102 | lld:pubmed |
| pubmed-article:1732169 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1732169 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1732169 | pubmed:pagination | 59-69 | lld:pubmed |
| pubmed-article:1732169 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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| pubmed-article:1732169 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1732169 | pubmed:articleTitle | The rec102 mutant of yeast is defective in meiotic recombination and chromosome synapsis. | lld:pubmed |
| pubmed-article:1732169 | pubmed:affiliation | Department of Biology, Yale University, New Haven, Connecticut 06511-8112. | lld:pubmed |
| pubmed-article:1732169 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1732169 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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