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    Safronova, L. D. and Chubykin, V. L. 2013. Meiotic drive in mice carrying t-complex in their genome. Russian Journal of Genetics, Vol. 49, Issue. 9, p. 885.

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    Schimenti, J. C. Reynolds, J. L. and Planchart, A. 2005. Mutations in Serac1 or Synj2 cause proximal t haplotype-mediated male mouse sterility but not transmission ratio distortion. Proceedings of the National Academy of Sciences, Vol. 102, Issue. 9, p. 3342.

    Lyon, Mary F. 2003. Transmission Ratio Distortion in Mice. Annual Review of Genetics, Vol. 37, Issue. 1, p. 393.

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    Fraser, Lynn R. and Dudley, Keith 1999. New insights into the t-complex and control of sperm function. BioEssays, Vol. 21, Issue. 4, p. 304.

    Braidotti, Giovanna and Barlow, Denise P. 1997. Identification of a male meiosis-specific gene, Tcte2, which is differentially spliced in species that form sterile hybrids with laboratory mice and deleted in t chromosomes showing meiotic drive. Developmental Biology, Vol. 186, Issue. 1, p. 85.

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    Olds-Clarke, Patricia Pilder, Stephen H. Visconti, Pablo E. Moss, Stuart B. Orth, Joanne M. and Kopf, Gregory S. 1996. Sperm from mice carrying twot haplotypes do not possess a tyrosine phosphorylated form of hexokinase. Molecular Reproduction and Development, Vol. 43, Issue. 1, p. 94.

    Silver, Lee M. and Buck, Christine 1993. The mouse t complex distorter-3 ( Tcd-3) locus and transmission ratio distortion. Genetical Research, Vol. 62, Issue. 02, p. 133.


Deletion of mouse t-complex distorter-1 produces an effect like that of the t-form of the distorter

  • Mary F. Lyon (a1)
  • DOI:
  • Published online: 01 April 2009

An allele of the mouse brachyury locus, T22H, had been shown previously to involve a deletion of several markers in the proximal part of chromosome 17, and almost certainly includes deletion of the t-complex distorter gene Tcd-1. The effects of T22H on transmission ratio distortion and male sterility caused by the t-complex were compared with those of a partial t-haplotype th51, which carries the t-form of the distorter Tcd-1t. In combination with the complete haplotypetf32, T22H caused severe impairment of male fertility, but males of genotype T22H/t6 or T22H/thSl were normally fertile. These results were very similar to those obtained when th51 was in combination with the same haplotypes. In effect on transmission ratio T22H was again similar to thSI, in that it produced a marked increase in the transmission of the haplotype t6. To test whether the effects of T22H were due to deletion of elements other than Tcd-1, the effect of T22H on transmission of the partial haplotype th2 was compared with that of the deletion Thv. Again T22H markedly increased transmission of the t-haplotype and the effect was significantly greater than the small effect produced by Thp.

It is concluded that deletion of the distorter Tcd-1 has an effect like that of the t-form of this distorter, Tcd-1t, and hence that Ted-11 must be an amorph or hypomorph. It is speculated that other t-complex distorters, Tcd-2t and Tcd-3t may also be amorphs or hypomorphs. Thus, the phenomena of transmission ratio distortion and male sterility due to the t-complex appear to be brought about by differential susceptibility of wild-type and t-responder alleles, Tcr+ and Tcrt, to a shortage of distorter gene product.

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Genetics Research
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