Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/ijms22042125
Keywords
bisphenol A; paternal exposure; histone acetylation; sperm epigenome; heart development
Funding
- Spanish Ministry of Economy and Competitiveness [AGL2014-53167-C3-3-R, BES-2015-071885]
- Fundacion Carolina Rodriguez (Universidad de Leon)
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Parental exposure to BPA has been linked to a greater incidence of congenital diseases. In zebrafish males, BPA induces an increase in sperm histone acetylation that is transmitted to unexposed progeny. Histone hyperacetylation promoted by paternal BPA exposure alters chromatin structure in progeny, leading to overexpression of genes involved in cardiogenesis.
Parental exposure to bisphenol A (BPA) has been linked to a greater incidence of congenital diseases. We have demonstrated that BPA induces in zebrafish males an increase in the acetylation of sperm histones that is transmitted to the blastomeres of the unexposed progeny. This work is aimed to determine whether histone hyperacetylation promoted by paternal exposure to BPA is the molecular mechanism underlying the cardiogenesis impairment in the descendants. Zebrafish males were exposed to 100 and 2000 mu g/L BPA during early spermatogenesis and mated with non-exposed females. We analyzed in the progeny the expression of genes involved in cardiogenesis and the epigenetic profile. Once the histone hyperacetylation was confirmed, treatment with epigallocatechin gallate (EGCG), an inhibitor of histone acetyltransferases, was assayed on F1 embryos. Embryos from males exposed to 2000 mu g/L BPA overexpressed the transcription factor hand2 and the receptor esr2b, showing their own promoters-as well as that of kat6a-an enrichment in H3K9ac. In embryos treated with EGCG, both gene expression and histone acetylation (global and specific) returned to basal levels, and the phenotype was recovered. As shown by the results, the histone hyperacetylated landscape promoted by BPA in the sperm alters the chromatin structure of the progeny, leading to the overexpression of the histone acetyltransferase and genes involved in cardiogenesis.
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