DMSO impairs the transcriptional program for maternal-to-embryonic transition by altering histone acetylation. (February 2020)

• Record Type: Journal Article
• Authors: Kang, Min-Hee; You, Seong-Yeob; Hong, Kwonho; Kim, Jin-Hoi
• Is Part Of: Biomaterials. Volume 230(2020)
• Publication Date: 2020-02
• Subjects: DMSO -- RNA-Seq -- Acetylation -- Epigenetics -- 2-cell block -- Mouse preimplantation embryo; Biomedical materials -- Periodicals; Biocompatible Materials -- Periodicals; Biomatériaux -- Périodiques; 610.28
• DOI: 10.1016/j.biomaterials.2019.119604
• Languages: English
• ISSNs: 0142-9612

Abstract

Abstract: Dimethyl sulfoxide (DMSO) is widely used in basic and clinical research, yet its toxicity and biocompatibility properties remain elusive. Here, we report that exposure of mouse zygotes to 2% DMSO perturbed the transcriptional program, critical for maternal-to-embryonic transition and provoked developmental arrest at the 2- or 4-cell stage. Mechanistically, DMSO decreased total protein acetylation in the 2-cell embryos but increased histone H3 and H4 acetylations, as well as p53, H3K9, and H3K27 acetylations. The epigenetic changes led to an altered expression pattern of 16.26% of total valid genes in DMSO-exposed embryos. Among the affected genes, expression of maternal and minor zygotic gene activation (ZGA) genes was enhanced, whereas the ubiquitin-proteasome system, major ZGA transcripts, embryonic gene activation, the cell cycle, and ribosomal biogenesis genes were suppressed. Therefore, we conclude that DMSO causes developmental arrest by disrupting maternal-to-embryonic transition; hence, caution should be exerted when using it as a solvent.