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Is p53 controlling spermatogenesis in male mice with the deletion on the Y chromosome?

Published online by Cambridge University Press:  12 July 2011

Tomasz Lech
Affiliation:
Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Cracow, Poland.
Aniela Golas*
Affiliation:
Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Cracow, Poland.
Jozefa Styrna
Affiliation:
Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Cracow, Poland.
*
All correspondence to: Aniela Golas. Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Cracow, Poland. Tel: +48 12 663 24 34. Fax: +48 12 634 37 16. e-mail: [email protected]

Summary

The aim of the study was to evaluate the influence of the chromosome Y structure and Trp53 genotype on semen quality parameters. Mice with partial deletion of the Y chromosome (B10.BR-Ydel) have severely altered sperm head morphology when compared with males that possess the complete Y chromosome (B10.BR). Control males from B10.BR and B10.BR-Ydel mice, and mutant males from B10.BR-p53−/− and B10.BR-Ydel-p53−/− experimental groups were used. We assessed testis weight, sperm head abnormalities, viability of spermatozoa (eosin test), percentage of motile and immature sperm, and performed a hypo-osmotic test to detect abnormal tail membrane integrity. Sperm morphology and maturation were controlled by the genes within the deleted region of the Y chromosome. Testis weight was higher in the mutants than in the control males, possibly due to cell accumulation in Trp53-deficient males as the concentration of sperm was significantly increased in the mutants. An elevated percentage of abnormal sperm was noted in B10.BR-p53−/− and B10.BR-Ydel-p53−/− male mice. We suggest that, in Trp53-deficient mice, the sperm cells that escape apoptosis are the ones that have abnormal morphology. The only sperm quality parameter affected by the interplay between Trp53 and chromosome Y genes was sperm motility, which was elevated in B10.BR-p53−/− males, but remained unchanged in B10.BR-Ydel-p53−/− males.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2011

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