| pubmed-article:1379333 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0000768 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0020205 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0013139 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0162788 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:1379333 | lifeskim:mentions | umls-concept:C1524063 | lld:lifeskim |
| pubmed-article:1379333 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1379333 | pubmed:dateCreated | 1992-9-1 | lld:pubmed |
| pubmed-article:1379333 | pubmed:abstractText | The purpose of this paper is the genetic visualization by in situ hybridization of 130 sex-linked recessive lethals plus a non-lethal induced by I-R dysgenesis. This collection of lethals involves inducer strains which differ in the position of the I elements on the X chromosomes. The I-R interaction was strong. Our previous results have shown that about 30% of the induced recessive lethals are associated with cytologically visible chromosomal rearrangements. (1) The rearrangements induced by I-R-type hybrid dysgenesis often exhibit homology with the I factor at the level of one or both junction points, depending on the types of chromosome rearrangements. These results suggest that the chromosome rearrangements arise directly from the transposition of I elements. However, the breakpoints of some types of cytologically non-visible deficiencies and of 2 small cytologically visible deficiencies do not present detectable homology with the I factor. (2) The majority of rearrangements do not involve the I elements already present on the paternal X chromosome. (3) The hybridization signal distributions on the X chromosome are not uniform. They present peaks of various heights which may correspond to specific anchoring areas of copies of I in the course of integration. (4) The data presented here agree with the literature with respect to the mean number of copies of I per X chromosome and to the excess of copies of I at locus 1A. Two rearrangement formation mechanisms are envisaged: crossing-over and 'target' exchanges. | lld:pubmed |
| pubmed-article:1379333 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1379333 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1379333 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1379333 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1379333 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1379333 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:1379333 | pubmed:issn | 0027-5107 | lld:pubmed |
| pubmed-article:1379333 | pubmed:author | pubmed-author:ProustJJ | lld:pubmed |
| pubmed-article:1379333 | pubmed:author | pubmed-author:PrudhommeauCC | lld:pubmed |
| pubmed-article:1379333 | pubmed:author | pubmed-author:GottelandMM | lld:pubmed |
| pubmed-article:1379333 | pubmed:author | pubmed-author:LadevèzeVV | lld:pubmed |
| pubmed-article:1379333 | pubmed:author | pubmed-author:Fontyne-Branc... | lld:pubmed |
| pubmed-article:1379333 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1379333 | pubmed:volume | 268 | lld:pubmed |
| pubmed-article:1379333 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1379333 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1379333 | pubmed:pagination | 265-85 | lld:pubmed |
| pubmed-article:1379333 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:1379333 | pubmed:meshHeading | pubmed-meshheading:1379333-... | lld:pubmed |
| pubmed-article:1379333 | pubmed:meshHeading | pubmed-meshheading:1379333-... | lld:pubmed |
| pubmed-article:1379333 | pubmed:meshHeading | pubmed-meshheading:1379333-... | lld:pubmed |
| pubmed-article:1379333 | pubmed:meshHeading | pubmed-meshheading:1379333-... | lld:pubmed |
| pubmed-article:1379333 | pubmed:meshHeading | pubmed-meshheading:1379333-... | lld:pubmed |
| pubmed-article:1379333 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1379333 | pubmed:articleTitle | I-R hybrid dysgenesis in Drosophila melanogaster. Use of in situ hybridization to show the association of I factor DNA with induced sex-linked recessive lethals. | lld:pubmed |
| pubmed-article:1379333 | pubmed:affiliation | Laboratoire de Biologie Générale, Université Paris-Sud, Orsay, France. | lld:pubmed |
| pubmed-article:1379333 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1379333 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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