Disruption of NNAT, NAP1L5 and MKRN3 DNA methylation and transcription in rabbit parthenogenetic fetuses.

Parthenogenetically activated oocytes cannot develop to term in mammals due to lack of paternal gene expression. Disruption of imprinted gene expression and DNA methylation status in parthenogenetic fetuses has been reported in mice and pigs, but not in rabbits. In this study, the genomic imprinting status of the paternally expressed genes Neuronatin ( NNAT ), Nucleosome assembly protein 1-like 5 ( NAP1L5 ), and Makorin ring finger protein 3 ( MKRN3 ) was compared between rabbit parthenogenetic (PA) and normally fertilized fetuses (Con) using quantitative real-time PCR (qRT-PCR) and bisulfite sequencing PCR (BSP). The results revealed a significantly reduced expression of NNAT , NAP1L5 , and MKRN3 in rabbit PA fetuses compared with Con fetuses ( p < 0.05). In addition, the BSP results demonstrated hypermethylation in the differentially methylated regions (DMRs) of NNAT , NAP1L5, and MKRN3 in rabbit PA fetuses. Taken together, these results suggest that hypermethylation of DMRs is associated with decreased NNAT , NAP1L5, and MKRN3 expression, which may be responsible for developmental failure of rabbit PA fetuses. [ABSTRACT FROM AUTHOR]