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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*
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.

Summary

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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
Copyright
Copyright © Cambridge University Press 1990

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