During initial development, both X chromosomes are active in females, and one of 
them must be silenced at the appropriate time in order to dosage compensate 
their gene expression levels to male counterparts. Silencing involves epigenetic 
mechanisms, including histone deacetylation. Major X chromosome inactivation 
(XCI) in bovine occurs between hatching and implantation, although in vitro 
culture conditions might disrupt the silencing process, increasing or decreasing 
X-linked gene expression. In this study, we aimed to address the roles of 
histone deacetylase inhibition by trichostatin A (TSA) on female preimplantation 
development. We tested the hypothesis that by enhancing histone acetylation, TSA 
would increase the percentage of embryos achieving 16-cell stage, reducing 
percentage of embryos blocked at 8-cell stage, and interfere with XCI in IVF 
embryos. We noticed that after TSA treatment, acetylation levels in individual 
blastomeres of 8-16 cell embryos were increased twofold on treated embryos, and 
the same was detected for blastocysts. Changes among blastomere levels within 
the same embryo were diminished on TSA group, as low-acetylated blastomeres were 
no longer detected. The percentage of embryos that reached the 5th cleavage 
cycle 118 h after IVF, analyzed by Hoechst staining, remained unaltered after 
TSA treatment. Then, we assessed XIST and G6PD expression in individual female 
bovine blastocysts by quantitative real-time PCR. Even though G6PD expression 
remained unaltered after TSA exposure, XIST expression was eightfold decreased, 
and we also detected a major decrease in the percentage of blastocysts 
expressing detectable XIST levels after TSA treatment. Based on these results, 
we conclude that HDAC is involved on XCI process in bovine embryos, and its 
inhibition might delay X chromosome silencing and attenuate aberrant XIST 
expression described for IVF embryos.