Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1928845 | Biochemical and Biophysical Research Communications | 2013 | 7 Pages |
•Histone modification of the mouse pronuclei is regulated by poly(ADP-ribosylation).•Hypermethylation of the mouse female pronuclei is maintained by poly(ADP-ribosylation).•Parp1 is physically interacted with Suz12, which may function in the pronuclei.•Poly(ADP-ribosylation) affects ultrastructure of chromatin of the mouse pronucleus.
We examined the roles of poly(ADP-ribosylation) in chromatin remodeling during the first cell cycle of mouse embryos. Drug-based inhibition of poly(ADP-ribosylation) by a PARP inhibitor, PJ-34, revealed up-regulation of dimethylation of histone H3 at lysine 4 in male pronuclei and down-regulation of dimethylation of histone H3 at lysine 9 (H3K9) and lysine 27 (H3K27). Association of poly(ADP-ribosylation) with histone modification was suggested to be supported by the interaction of Suz12, a histone methyltransferase in the polycomb complex, with Parp1. PARP activity was suggested to be required for a proper localization and maintenance of Suz12 on chromosomes. Notably, DNA methylation level of female pronuclei in one-cell embryos was robustly decreased by PJ-34. Electron microscopic analysis showed a frequent appearance of unusual electron-dense areas within the female pronuclei, implying the disorganized and hypercondensed chromatin ultrastructure. These results show that poly(ADP-ribosylation) is important for the integrity of non-equivalent epigenetic dynamics of pronuclei during the first cell cycle of mouse embryos.