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New insights into the t ‐complex and control of sperm function
Author(s) -
Fraser Lynn R.,
Dudley Keith
Publication year - 1999
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(199904)21:4<304::aid-bies6>3.0.co;2-h
Subject(s) - biology , capacitation , sperm , gene , genetics , x chromosome , male infertility , y chromosome , chromosome , population , sperm motility , infertility , medicine , pregnancy , environmental health
The mouse t ‐complex, located on chromosome 17, contains genes known to influence male, but not female, fertility. Although some t ‐complex genes are recessive lethals, t ‐chromosomes are maintained in the population by transmission ratio distortion. When male mice heterozygous for the t ‐chromosome mate with wild‐type females, most offspring will possess the t ‐chromosome, indicating a link between t ‐complex genes and sperm function. Several proteins coded for by t ‐complex genes have been localised in the sperm flagellum, suggesting roles relating to motility. Another t ‐complex protein appears able to regulate the adenylyl cyclase/cAMP signal transduction pathway, known to play an important role in capacitation. Defective motility and/or failure to capacitate (“switch on”) would result in poorly fertile or infertile spermatozoa. Given the existence of human homologues for many genes in the t ‐complex and the prevalence of “male factor” infertility, information obtained about the t ‐complex not only will provide insight into basic biological mechanisms but may be of future clinical relevance as well. BioEssays 21:304–312, 1999. © 1999 John Wiley & Sons, Inc.