Mouse Chromosome 17

Silver, Lee M.; Artzt, Karen; Barlow, Denise P.; Fischer-Lindahl, Kirsten; Lyon, Mary F.; Klein, Jan; Snyder, Linda C.

doi:10.1007/bf00648435

Cited by 37 publications

(2 citation statements)

References 189 publications

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“…have been discredited (Lyon 1984), but the view that tcp-1 might be tcd-4 is still valid (Silver et al 1992). However, not only is the relation between tcp-1 and tcd-4 uncertain, but the involvement of tcd-4 in distortion is also ambiguous.…”

Section: A M O D E L F O R T H E a C T Io N Of T H E C O M P L E Xmentioning

confidence: 99%

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A model for the mechanism of transmission ratio distortion and fort-associated hybrid sterility

Hurst

1993

Proc. R. Soc. Lond. B

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A mechanistic model is presented to account for the action of t-complex of mice. This model takes account of recent evidence suggesting that t-complex distorters are amorphs or hypomorphs. Following Lyon's (Genet. Res. 59, 27 (1992) scheme, the model proposes that the t-complex distorter (tcd+) loci for normal function than does the wild-type form of tcr. However, a tradeoff against this ability to drive is a reduced efficiency of the haploid specific product of tcrt in the absence of drive. Regulation of tcr could be achieved by differential splicing or post-translational modification under the control of the t-complex distorters. It is shown that the model is consistent with known fertility and distortion data, as well as with the finding that the mechanism of drive is intimately connected with the mechanism of intraspecific homozygous sterility. Importantly, the model predicts that the mechanism of hybrid sterility associated with the t-complex is the same as the mechanism of intraspecific homozygous sterility. If accepted then this will be, to the best of the author's knowledge, the first description and characterization of a Haldane rule sterility gene. The new understanding of the mechanisms of t-complex shows its mode of operation to be fundamentally different to the only other well-described autosomal meiotic driver, Segregation Distorter (SD) of Drosophila melanogaster.

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Section: A M O D E L F O R T H E a C T Io N Of T H E C O M P L E Xmentioning

confidence: 99%

“…In models of the action of t r d before 1992 (discussed in Lyttle 1991) it was typically assumed that the D1 loci were producing some product that was toxic to sperm. Silver et al 1992). The location of genes are shown in parentheses after the gene name.…”

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confidence: 99%

A model for the mechanism of transmission ratio distortion and fort-associated hybrid sterility

Hurst

1993

Proc. R. Soc. Lond. B

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TheMASProto-Oncogene Is Not Imprinted in Humans

et al. 1996

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Linkage mapping of the cystathionine ?-synthase (CBS) gene on human chromosome 21 using a DNA polymorphism in the 3? untranslated region

et al. 1993

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We used single-strand conformation polymorphism (SSCP) to detect DNA polymorphisms in the 3' untranslated (3'UT) region of the gene for cystathionine beta-synthase (CBS). A polymorphism due to a T-to-C substitution at nucleotide 549 of the 3'UT region with heterozygosity of 46% has been identified. Genotypes for this polymorphism have been obtained in all of the informative CEPH families, and CBS has been placed in the linkage map of human chromosome 21.

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Mouse Chromosome 17

Cited by 37 publications

References 189 publications

A model for the mechanism of transmission ratio distortion and fort-associated hybrid sterility

A model for the mechanism of transmission ratio distortion and fort-associated hybrid sterility

TheMASProto-Oncogene Is Not Imprinted in Humans

Linkage mapping of the cystathionine ?-synthase (CBS) gene on human chromosome 21 using a DNA polymorphism in the 3? untranslated region

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