Deletion of paternal ventral prostate gland leads to aberrant methylation of embryonic genome in the golden hamster

Abstract

In the golden hamster, deletion of paternal ventral prostate gland (VPG) predisposes to abnormalities and lethality of sired embryos even though fertilization rate is normal. To explain this, we propose that reprogramming of paternal genome is disturbed because sperm are not in contact with ventral prostate gland secretions at mating. We studied methylation status of epididymal sperm, uterine sperm (ejaculated sperm) and perinatal foetuses by Southern blotting. We also studied total methylation in decondensed sperm and nuclei of pronuclear stage zygotes by staining with anti 5-methylcytidine. Data were analysed with Student t-test. Compared with the control (SH Group) methylation of the paternally imprinted gtl2 and H19 in sperm collected from epididymis and uterus of VPX (males with bilateral deletion of ventral prostate gland) group was not changed. gtl2 promoter in D13 embryos of VPX group was less methylated (p<0.05). Even though no statistical difference could be detected, methylation of the H19 promoter of VPX embryos was found to fluctuate substantially. Overall methylation in decondensed sperm between the two groups did not differ but male pronuclei of the VPX group zygotes were less methylated compared with the control (p<0.01). Therefore aberrant methylation may account for abnormal development of embryos derived from sperm not exposed to VPG secretions.