PMID- 10501965
OWN - NLM
STAT- MEDLINE
DCOM- 20000203
LR  - 20190905
IS  - 0938-8990 (Print)
IS  - 0938-8990 (Linking)
VI  - 10
IP  - 10
DP  - 1999 Oct
TI  - ORFless, intronless, and mutant transcription units in the mouse t complex
      responder (Tcr) locus.
PG  - 969-76
AB  - 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.
FAU - Schimenti, J C
AU  - Schimenti JC
AD  - The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
LA  - eng
SI  - GENBANK/AF140707
SI  - GENBANK/AF140708
SI  - GENBANK/AF140709
SI  - GENBANK/AF140710
SI  - GENBANK/AF141019
GR  - CA34196/CA/NCI NIH HHS/United States
GR  - HD24374/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mamm Genome
JT  - Mammalian genome : official journal of the International Mammalian Genome Society
JID - 9100916
RN  - 0 (Genetic Markers)
RN  - 0 (Gpr31 protein, mouse)
RN  - 0 (Proteins)
RN  - 0 (Receptors, Cytokine)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Ribosomal Protein S6)
RN  - 0 (Ribosomal Proteins)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.11.1 (Ribosomal Protein S6 Kinases)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Chromosome Mapping
MH  - Chromosomes/*genetics
MH  - Cloning, Molecular
MH  - Genetic Markers
MH  - Haplotypes/*genetics
MH  - Introns/*genetics
MH  - Mice
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Open Reading Frames/*genetics
MH  - Protein Kinases/chemistry/genetics
MH  - Proteins/chemistry/genetics
MH  - Receptors, Cytokine/chemistry/genetics
MH  - *Receptors, G-Protein-Coupled
MH  - Recombination, Genetic
MH  - Ribosomal Protein S6
MH  - Ribosomal Protein S6 Kinases/chemistry/genetics
MH  - Ribosomal Proteins/metabolism
MH  - Sequence Alignment
MH  - Transcription, Genetic/*genetics
EDAT- 1999/09/29 00:00
MHDA- 1999/09/29 00:01
CRDT- 1999/09/29 00:00
PHST- 1999/09/29 00:00 [pubmed]
PHST- 1999/09/29 00:01 [medline]
PHST- 1999/09/29 00:00 [entrez]
AID - MGS2146 [pii]
AID - 10.1007/s003359901142 [doi]
PST - ppublish
SO  - Mamm Genome. 1999 Oct;10(10):969-76. doi: 10.1007/s003359901142.