caa a22 4500 469061928 CHVBK 20180323132900.0 cr unu---uuuuu 170328e19921001xx s 000 0 eng 10.1007/BF00350625 doi (NATIONALLICENCE)springer-10.1007/BF00350625 Functional analysis of a t complex responder locus transgene in mice [Elektronische Daten] [Daniel Bullard, Christine Ticknor, John Schimenti] Transmission ratio distortion (TRD) of mouse t haplotypes occurs through the interaction of multiple distorter loci with the t complex responder (Tcr) locus. Males heterozygous for a t haplotype will transmit the t-bearing chromosome to nearly all of their offspring. This process is mediated by the production of functionally inequivalent gametes: wildtype meiotic partners of t spermatozoa are rendered functionally inactive. The Tcr locus, which is required for TRD to occur, is thought to somehow protect its host spermatid from the sperm-inactivating effects of linked distorter genes (Lyon 1984). In previous work, Tcr was mapped to a small genetic interval in t haplotypes, and a candidate gene from this region was isolated (Tcp-10b t). In this work, we further localize Tcr to a 40-kb region that contains the 21-kb Tcp-10b t gene. A cloned genomic copy of Tcp-10b t was used to generate transgenic mice. The transgene was bred into a variety of genetic backgrounds to test for non-Mendelian segregation. Abberrant segregation was observed in some mice carrying either a complete t haplotype or a combination of certain partial t haplotypes. These observations, coupled with those of Snyder and colleagues (in this issue), provide genetic and functional evidence that the Tcp-10b t gene is Tcr. However, other genotypes that were predicted to produce distortion did not. The unexpected data from a variety of crosses in this work and those of our colleagues suggest that elements to the TRD system and the Tcr locus remain to be identified. Springer-Verlag New York Inc, 1992 Bullard Daniel Institute for Molecular Genetics, Baylor College of Medicine, One Baylor Plaza, 77030, Houston, Texas, USA aut Ticknor Christine Department of Genetics, Case Western Reserve University, School of Medicine, 44106, Cleveland, Ohio, USA aut Schimenti John Department of Genetics, Case Western Reserve University, School of Medicine, 44106, Cleveland, Ohio, USA aut Mammalian Genome Springer-Verlag 3/10(1992-10-01), 579-587 0938-8990 3:10<579 1992 3 335 https://doi.org/10.1007/BF00350625 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00350625 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Bullard Daniel Institute for Molecular Genetics, Baylor College of Medicine, One Baylor Plaza, 77030, Houston, Texas, USA aut NATIONALLICENCE 700 1- Ticknor Christine Department of Genetics, Case Western Reserve University, School of Medicine, 44106, Cleveland, Ohio, USA aut NATIONALLICENCE 700 1- Schimenti John Department of Genetics, Case Western Reserve University, School of Medicine, 44106, Cleveland, Ohio, USA aut NATIONALLICENCE 773 0- Mammalian Genome Springer-Verlag 3/10(1992-10-01), 579-587 0938-8990 3:10<579 1992 3 335 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer