
doi: 10.1038/349239a0
pmid: 1987476
Mouse t haplotypes represent a variant form of chromosome 17 that has evolved the ability to propagate through natural populations by the phenomenon of 'transmission ratio distortion' (TRD), in which heterozygous +/t males transmit their t-carrying chromosome to 95% or more of their offspring. Although multiple t-associated loci have a role in expression of this phenotype, only one--the t complex responder (Tcr) locus--is responsible for determining which of the two homologues of chromosome 17 will be transmitted at a high ratio. A candidate gene (Tcp-10b) for Tcr that is expressed in both meiotic and post-meiotic male germ cells has been cloned. But for this candidate gene to function as the haploid effector of TRD, the t-allele of this gene (Tcp-10bt) must express a unique product in a haploid-specific manner. Here we show that a change in the splicing pattern of Tcp-10bt transcripts occurs during sperm differentiation. This change results in a unique allele-specific and haploid-specific transcript which could encode a variant polypeptide that would fulfil the conditions required of the Tcr effector of TRD.
Male, Base Sequence, RNA Splicing, Molecular Sequence Data, Mitosis, Polymerase Chain Reaction, Chromosomes, Meiosis, Mice, Phenotype, Gene Expression Regulation, Haplotypes, Genes, Regulator, Animals, Amino Acid Sequence, RNA, Messenger, Spermatogenesis, Alleles
Male, Base Sequence, RNA Splicing, Molecular Sequence Data, Mitosis, Polymerase Chain Reaction, Chromosomes, Meiosis, Mice, Phenotype, Gene Expression Regulation, Haplotypes, Genes, Regulator, Animals, Amino Acid Sequence, RNA, Messenger, Spermatogenesis, Alleles
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