Linked Life Data

1794053

Source:http://linkedlifedata.com/resource/pubmed/id/1794053

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1992-4-9
pubmed:abstractText
The suppression of crossing-over and the consequent linkage disequilibrium of genetic markers within the t complex of the house mouse is caused by two large and two short inversions. The inversions encompass a region that is some 15 centiMorgans (cM) long in the homologous wild-type chromosome. The limits of the proximal inversions are reasonably well-defined, those of the distal inversions much less so. We have recently obtained seven new DNA markers (D17Tu) which in wild-type chromosomes map into the region presumably involved in the distal inversions of the t chromosomes. To find out whether the corresponding loci do indeed reside within the inversions, we have determined their variability among 26 complete and 12 partial t haplotypes. In addition, we also tested the same collection of t haplotypes for their variability at five D17Leh, Hba-ps4, Pim-1, and Crya-1 loci. The results suggest that the distal end of the most distal inversion lies between the loci D17Leh467 and D17Tu26. The proximal end of the large distal inversion was mapped to the region between the D17Tu43 and Hba-ps4 loci, but this assignment is rather ambiguous. The loci Pim-1, Crya-1, and the H-2 complex, which have been mapped between the Hba-ps4 and Grr within the large distal inversion, behave as if they recombine from time to time with their wild-type homologs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0938-8990
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
242-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Limits of the distal inversion in the t complex of the house mouse: evidence from linkage disequilibria.
pubmed:affiliation
Abteilung Immungenetik, Max-Planck-Institut für Biologie, Tübingen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't