Abstract
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 offspring1,2. 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 ratio3. A candidate gene (Tcp-10b) for Tcr that is expressed in both meiotic and post-meiotic male germ cells has been cloned4. 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 ofTcp-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.
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Cebra-Thomas, J., Decker, C., Snyder, L. et al. Allele- and haploid-specific product generated by alternative splicing from a mouse t complex responder locus candidate. Nature 349, 239–241 (1991). https://doi.org/10.1038/349239a0
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DOI: https://doi.org/10.1038/349239a0
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