pubmed-article:2657397 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2657397 | lifeskim:mentions | umls-concept:C0036025 | lld:lifeskim |
pubmed-article:2657397 | lifeskim:mentions | umls-concept:C0085187 | lld:lifeskim |
pubmed-article:2657397 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
pubmed-article:2657397 | lifeskim:mentions | umls-concept:C0162326 | lld:lifeskim |
pubmed-article:2657397 | lifeskim:mentions | umls-concept:C1875307 | lld:lifeskim |
pubmed-article:2657397 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:2657397 | pubmed:dateCreated | 1989-7-5 | lld:pubmed |
pubmed-article:2657397 | pubmed:abstractText | The termini of Saccharomyces cerevisiae chromosomes consist of tracts of C1-3A (one to three cytosine and one adenine residue) sequences of approximately 450 base pairs in length. To gain insights into trans-acting factors at telomeres, high-copy-number linear and circular plasmids containing tracts of C1-3A sequences were introduced into S. cerevisiae. We devised a novel system to distinguish by color colonies that maintained the vector at 1 to 5, 20 to 50, and 100 to 400 copies per cell and used it to change the amount of telomeric DNA sequences per cell. An increase in the number of C1-3A sequences caused an increase in the length of telomeric C1-3A repeats that was proportional to plasmid copy number. Our data suggest that telomere growth is inhibited by a limiting factor(s) that specifically recognizes C1-3A sequences and that this factor can be effectively competed for by long tracts of C1-3A sequences at telomeres or on circular plasmids. Telomeres without this factor are exposed to processes that serve to lengthen chromosome ends. | lld:pubmed |
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pubmed-article:2657397 | pubmed:language | eng | lld:pubmed |
pubmed-article:2657397 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2657397 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2657397 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2657397 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2657397 | pubmed:month | Apr | lld:pubmed |
pubmed-article:2657397 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:2657397 | pubmed:author | pubmed-author:ZakianV AVA | lld:pubmed |
pubmed-article:2657397 | pubmed:author | pubmed-author:RungeK WKW | lld:pubmed |
pubmed-article:2657397 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2657397 | pubmed:volume | 9 | lld:pubmed |
pubmed-article:2657397 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2657397 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2657397 | pubmed:pagination | 1488-97 | lld:pubmed |
pubmed-article:2657397 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:2657397 | pubmed:meshHeading | pubmed-meshheading:2657397-... | lld:pubmed |
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pubmed-article:2657397 | pubmed:meshHeading | pubmed-meshheading:2657397-... | lld:pubmed |
pubmed-article:2657397 | pubmed:year | 1989 | lld:pubmed |
pubmed-article:2657397 | pubmed:articleTitle | Introduction of extra telomeric DNA sequences into Saccharomyces cerevisiae results in telomere elongation. | lld:pubmed |
pubmed-article:2657397 | pubmed:affiliation | Fred Hutchinson Cancer Research Center, Seattle, Washington 98104. | lld:pubmed |
pubmed-article:2657397 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2657397 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2657397 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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