Correlation of centromeric heterochromatin C-band polymorphism with breeding failure in mice

The aim of the present study was to test the hypothesis about the relation between segregation of chromosomes 14 and 18 and the deterioration of mouse fertility and vitality. The analysis was possible because C-banding on chromosome 14 and chromosome 18 of the CBA/Kw and KE strains show size polymorphism. A small sized C-band on chromosome 14 is characteristic for the CBA/Kw mice, while the KE mice show small C-bands on chromosomes 18. Thus, if fertility parameters are affected in a centromere-dependent manner, we should observe non-random inheritance of both chromosome pairs in recombinant inbred (RI) strains. The results showed statistically significant preferential segregation of chromosomes 14 and 18 with small C-bands. Most of the RI strains inherited chromosome 14 from the CBA/Kw strain and chromosome 18 from the KE strain, and did not manifest a deterioration of fertility and vitality. On the contrary, RI strains that inherited chromosomes 14 and 18 from one of the parental strains, particularly the KE strain, stopped breeding or had difficulties in producing the next generation

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

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-Y-del) 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-Y-del mice, and mutant males from B10.BR-p53(-/-) and B10.BR-Y-del-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-Y-del-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-Y-del-p53(-/-) males

Reproductive capacity of male bank voles (Myodes glareolus SCHREBER, 1780) : age-dependent changes in functional activity of epididymal sperm

The influence of age on male bank voles’ reproductive tract development, epididymal sperm quantity and functional activity was investigated. Experiments were carried out on male bank voles aged 1.5 to 15 months (n=10 each in 8 age groups). The developmental stage of the reproductive tract was assessed by the weight of testes, seminal vesicles and coagulation glands. In each age group the number of epididymal sperm and their functional activity were examined. Epididymal sperm functional activity was assessed by motility, viability, maturity, head morphology and integrity of the sperm tail membrane. Ageing males were heavier than pre-pubertal and mature ones. Male age also affected the testes, seminal vesicles and coagulation gland development. The heaviest accessory sex glands were noted in 3-month-old males and the lightest in prepubertal (1.5-month-old) and older (12- and 15-month-old) males. Sperm counts were significantly higher in 3-, 4- and 5-month-old males than in pre-pubertal and old males. Generally, adult males aged 3- and 4- months, produced sperm of better functional activity. In conclusion, the best male reproductive capacity is found in bank voles of 3 to 4 months of age