Hostname: page-component-cd9895bd7-lnqnp Total loading time: 0 Render date: 2024-12-26T16:19:06.236Z Has data issue: false hasContentIssue false
  • English
  • Français

Elevated galactosyltransferase activity on t-bearing sperm segregates with T/t-complex distorter loci-2

Published online by Cambridge University Press:  14 April 2009

Barry D. Shur  and
Natalie F. Scully
Barry D. Shur*
Affiliation:
Department of Biochemistry and Molecular Biology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030
Natalie F. Scully
Affiliation:
Department of Biochemistry and Molecular Biology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030
*
* To whom correspondence should be addressed: Box 117, Biochemistry and Molecular Biology, M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030.
Rights & Permissions [Opens in a new window]

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Sperm bearing complete t-haplotypes are preferentially transmitted during fertilization from heterozygous +/t males, often in excess of 95% relative to their +-bearing meiotic partner. Sperm from t-bearing males have an approximate two- to fourfold increase in β1, 4-galactosyltransferase (GalTase) activity, a cell surface protein that mediates sperm binding to the egg zona pellucida. The elevated GalTase activity strictly correlates with the preferential transmission of t-sperm from +/t males, since eight other enzymes show normal levels of activity on t-sperm. Furthermore, sperm bearing proximal partial t-haplotypes, which are no longer favoured during fertilization, have normal levels of GalTase activity. Nevertheless, it has been unclear whether the elevated sperm GalTase activity on t-sperm is due to specific loci in the distal segment of the T/t-complex, or rather, is an indirect consequence of the abnormal sperm function characteristic of +/t and tx/ty males. In this study, it is shown that the elevated sperm GalTase activity is due specifically to factors that reside within the distal segment of the T/t complex, which also contains Tcd-2, the strongest of the distorter loci. Since the structural locus for GalTase is located on mouse chromosome 4, these results also show that T/t-complex alleles on chromosome 17 are regulatory in nature and affect the expression of sperm surface components critical for normal fertilization. Models are presented to explain how elevated GalTase activity could contribute to sperm transmission distortion.

Type
Research Article
Information
Genetics Research , Volume 55 , Issue 3 , June 1990 , pp. 177 - 181
Copyright
Copyright © Cambridge University Press 1990

References

Bennett, D. (1975). The T-locus of the mouse. Cell 6, 441–454.CrossRefGoogle Scholar
Brown, J., Cebra-Thomas, J. A., Bleil, J. D., Wassarman, P. M. & Silver, L. M. (1990). A premature acrosome reaction is programmed by mouse t haplotypes during sperm differentiation and could play a role in transmission ratio distortion. Development (in the press).Google Scholar
Furukawa, K., Roth, S. & Sawicki, J. (1986). Several galactosyltransferase activities are associated with mouse chromosome 17. Genetics 114, 983–991.CrossRefGoogle ScholarPubMed
Hashimoto, Y., Abe, M., Suzuki, A., Iwasaki, K. & Yamakawa, T. (1985). A locus controlling the activity of UDP-galactose: GM2 (NeuGy) galactosyltransferase in mouse liver is linked to the H-2 complex. Glycoconjugate Journal 2, 255–265.CrossRefGoogle Scholar
Kemp, J. D., Weinfeld, H. M. & Koerner, T. A. W. (1987). A quantitative analysis of H-2 linked effects on hepatic ganglioside composition. Immunogenetics 26, 130–137.CrossRefGoogle ScholarPubMed
Lopez, L. C, Bayna, E. M., Litoff, D., Shaper, N. L., Shaper, J. H. & Shur, B. D. (1985). The receptor function of mouse sperm surface galactosyltransferase during fertilization. Journal of Cell Biology 101, 1501–1510.CrossRefGoogle ScholarPubMed
Lyon, M. F. (1984). Transmission ratio distortion in mouse t-haplotypes is due to multiple distorter genes acting on a responder locus. Cell 37, 621–628.CrossRefGoogle ScholarPubMed
Lyon, M. F. (1986). Male sterility of the mouse t-complex is due to homozygosity of the distorter genes. Cell 44, 357–363.CrossRefGoogle ScholarPubMed
Olds-Clarke, P. (1989). Sperm from tw32/+ mice: capacitation is normal, but hyperactivation is premature and non-hyperactivated sperm are slow. Developmental Biology 131, 475–482.CrossRefGoogle Scholar
Olds-Clarke, P. & Peitz, B. (1985). Fertility of sperm from t/+ mice; evidence that +-bearing sperm are dysfunctional. Genetical Research 47, 49–52.CrossRefGoogle Scholar
Scully, N. F. & Shur, B. D. (1988). Stage specific increase in surface galactosyltransferase activity during spermatogenesis in t-bearing mice. Developmental Biology 125, 195–199.CrossRefGoogle Scholar
Seitz, A. W. & Bennett, D. (1985). Transmission distortion of t haplotypes is due to interactions between meiotic partners. Nature, London 313, 143–144.CrossRefGoogle ScholarPubMed
Shaper, N. L., Shaper, J. H., Hollis, G. F., Chang, H., Kirsch, I. R. & Kozak, C. A. (1987). The gene for galactosyltransferase maps to mouse chromosome 4. Cytogenetics and Cell Genetics 44, 18–21.CrossRefGoogle ScholarPubMed
Shur, B. D. (1981). Galactosyltransferase activities on mouse sperm bearing multiple tlethal and tviable haplotypes of the T/t-complex. Genetical Research 38, 225–236.CrossRefGoogle ScholarPubMed
Shur, B. D. & Bennett, D. (1979). A specific defect in galactosyltransferase regulation on sperm bearing mutant alleles of the T/t locus. Developmental Biology 71, 243–259.CrossRefGoogle ScholarPubMed
Shur, B. D. & Hall, N. G. (1982 a). Sperm surface galactosyltransferase activities during in vitro capacitation. Journal of Cell Biology 95, 567–573.CrossRefGoogle ScholarPubMed
Shur, B. D. & Hall, N. G. (1982 b). A role for mouse sperm surface galactosyltransferase in sperm binding to the egg zona pellucida. Journal of Cell Biology 95, 574–579.CrossRefGoogle Scholar
Shur, B. D. & Neely, C. A. (1988). Plasma membrane association, purification and characterization of mouse sperm β1, 4-galactosyltransferase. Journal of Biological Chemistry 263, 17706–17714.CrossRefGoogle Scholar
Silver, L. M. (1985). Mouse t haplotypes. Annual Review of Genetics 19, 179–208.CrossRefGoogle ScholarPubMed
Silver, L. M. (1990). Gene dosage effects on transmission ratio distortion by mouse t haplotypes. Genetical Research (in the press).Google Scholar
Silver, L. M., Kleene, K. C, Distel, R. J. & Hecht, N. B. (1987). Synthesis of mouse t-complex proteins during haploid stages of spermatogenesis. Developmental Biology 119, 605–608.CrossRefGoogle ScholarPubMed
Silver, L. M. & Remis, D. (1987). Five of the nine genetically defined regions of mouse t haplotypes are involved in transmission ratio distortion. Genetical Research 49, 51–56.CrossRefGoogle ScholarPubMed
Silver, L. M., Uman, J., Danska, J. & Garrels, J. I. (1983). A diversified set of testicular proteins specified by genes within the mouse t complex. Cell 35, 35–45.CrossRefGoogle ScholarPubMed