ArticleGenetics1996
Targeted mutagenesis of a candidate t complex responder gene in mouse t haplotypes does not eliminate transmission ratio distortion.
Article in Genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Identification of TCP10L as primate-specific gene derived via segmental duplication and homodimerization of TCP10L through the leucine zipper motif.Molecular biology reports · 2008Article
- LC2, the chlamydomonas homologue of the t complex-encoded protein Tctex2, is essential for outer dynein arm assembly.Molecular biology of the cell · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Transmission ratio distortion (TRI) associated with mouse t haplotypes causes +/t males to transmit the t-bearing chromosome to nearly all their offspring. Of the several genes involved in this phenomenon, the t complex responder (Tcrt) locus is absolutely essential for TRD to occur. A candidate Tcrt gene called Tcp10bt was previously cloned from the genetically defined Tcrt region. Its location, restricted expression in testis, and a unique postmeiotic alternative splicing pattern supported the idea that Tcp10bt was Tcrt. To test this hypothesis in a functional assay, ES cells were derived from a viable partial t haplotype, and the Tcp10bt gene was mutated by homologous recombination. Mutant mice were mated to appropriate partial t haplotypes to determine whether the targeted chromosome exhibited transmission ratios characteristic of the responder. The results demonstrated that the targeted chromosome retained full responder activity. Hence, Tcp10bt does not appear to be Tcrt. These and other observations necessitate a reevaluation of genetic mapping data and the actual nature of the responder.
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Registered trials
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