Linked Life Data

10501965

Source:http://linkedlifedata.com/resource/pubmed/id/10501965

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2000-2-3
pubmed:databankReference
pubmed:abstractText
Mouse t haplotypes exhibit transmission ratio distortion (TRD), whereby heterozygous males (+/t) transmit the t chromosome to nearly all offspring. TRD is mediated by the t complex responder locus (Tcr), whose transmission is elevated above Mendelian levels by additive contribution of several t haplotype-encoded quantitative trait loci (QTLs) called t complex distorters (Tcd1-Tcd5). The entire genetically defined Tcr interval has been cloned and consists of under 200 kb. This interval is one of three large duplication units in t haplotypes that retain high levels of similarity. The cis-active nature of Tcr raises the possibility that it is not a protein-encoding gene, but another anomaly such as a structural anomaly of chromatin. To further investigate the Tcr-critical interval, a 30-kb region upstream of the Tcp10b(t) gene (a testis-expressed former candidate for Tcr) was sequenced, along with the duplicated paralogous region associated with Tcp10c(t), which lies immediately adjacent but outside the Tcr interval. Several genes or transcriptional units were identified, including the 3' end of ribosomal s6 kinase (Rsk3); two apparently intronless and ORF-less genes; and Gpr31, an intronless, putative G-protein coupled receptor. While the 30-kb regions were 98% identical, the Gpr31 paralog from the Tcr-critical region (Gpr31b(t)) contained an in-frame 210-bp deletion that disrupted two of the seven predicted transmembrane domains. Furthermore, an intronless and ORFless gene from this interval, Trex1b(t), contained a 4-bp deletion that distinguished it from all other homologs in t haplotypes and wild-type chromosomes. Although it is unknown whether any of these genes are involved in TRD, their discovery raises new possibilities regarding the nature of Tcr, including a model whereby it might function as an RNA rather than a protein or chromatin anomaly.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0938-8990
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
969-76
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10501965-Amino Acid Sequence, pubmed-meshheading:10501965-Animals, pubmed-meshheading:10501965-Chromosome Mapping, pubmed-meshheading:10501965-Chromosomes, pubmed-meshheading:10501965-Cloning, Molecular, pubmed-meshheading:10501965-Genetic Markers, pubmed-meshheading:10501965-Haplotypes, pubmed-meshheading:10501965-Introns, pubmed-meshheading:10501965-Mice, pubmed-meshheading:10501965-Molecular Sequence Data, pubmed-meshheading:10501965-Mutation, pubmed-meshheading:10501965-Open Reading Frames, pubmed-meshheading:10501965-Protein Kinases, pubmed-meshheading:10501965-Proteins, pubmed-meshheading:10501965-Receptors, Cytokine, pubmed-meshheading:10501965-Receptors, G-Protein-Coupled, pubmed-meshheading:10501965-Recombination, Genetic, pubmed-meshheading:10501965-Ribosomal Protein S6, pubmed-meshheading:10501965-Ribosomal Protein S6 Kinases, pubmed-meshheading:10501965-Ribosomal Proteins, pubmed-meshheading:10501965-Sequence Alignment, pubmed-meshheading:10501965-Transcription, Genetic
pubmed:year
1999
pubmed:articleTitle
ORFless, intronless, and mutant transcription units in the mouse t complex responder (Tcr) locus.
pubmed:affiliation
The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.