Since discovery of dimethyl sulfoxide (DMSO), it has been applied to the multidisciplinary studies for basic and clinic research; yet its toxicity versus biocompatibility is poorly understood, leading to our inability to discover etiology behind its paradox. Here, we found that exposure of 2% DMSO to mouse zygotes caused developmental arrest at 2/4-cell embryos, and showed a decreased total acetylation levels. Besides, H3, H4, p53, H3K9, and H3K27 acetylation levels at DMSO-exposed 2-cell embryos are significantly increased. This affected the male pronucleus more than female. Further, RNA-sequence data demonstrates that DMSO alters approximately 16.26% transcripts of 2-cell embryos. Among them, maternal and minor zygotic gene activation (ZGA) transcripts are highly increased, whereas ubiquitin-proteasome system, major ZGA, embryonic gene activation, cell cycle, and ribosomal biogenesis transcripts are significantly down-regulated. These results suggest that DMSO caused developmental arrest by disrupting maternal-to-embryonic transition due to low proteasome activity and epigenetic alternations. SOURCE: Min-Hee Kang (minheekang312@gmail.com) - Jin-Hoi Kim Lab Konkuk University

Pluto Bioinformatics

GSE124598: Differentially expressed genes by DMSO in mouse 2-cell embryos identified by RNA sequencing