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The CHD family of proteins is characterized by the presence of chromodomains and SNF2-related helicase/ATPase domains, which alter gene expression by modification of chromatin structure. Chd1-null embryos arrest at the peri-implantation stage in mice. However, the functional role of CHD1 during preimplantation development remains unclear given maternal derived CHD1 may mask the essential role of CHD1 during this stage in traditional knockout models. The objective of this study was to characterize CHD1 expression and elucidate its functional role in preimplantation development using the bovine model. CHD1 mRNA was elevated after meiotic maturation and remains increased through 16-cell stage followed by a sharp decrease at morula to blastocyst stage. Similarly, immunoblot analysis indicated CHD1 protein level is increased after maturation, maintained at high level after fertilization and declined sharply afterwards. CHD1 mRNA level was partially decreased in response to α-amanitin (RNA polymerase II inhibitor) treatment, suggesting CHD1 mRNA in 8-cell embryos is of both maternal and zygotic origin. Results of siRNA-mediated silencing of CHD1 in bovine early embryos demonstrated that percentage of embryos developing to 8- to 16-cell and blastocyst stages were both significantly reduced. However, expression of NANOG (inner cell mass marker) and CDX2 (trophectoderm marker) were not affected in CHD1 knockdown blastocysts. In addition, we found that histone variant H3.3 immunostaining is altered in CHD1 knockdown embryos. Knockdown of H3.3 using siRNA resulted in a similar phenotype as CHD1 ablated embryos. Collectively, our results demonstrated that CHD1 is required for bovine early development and suggests that CHD1 may regulate H3.3 deposition during this period.

CHD1 Regulates Deposition of Histone Variant H3.3 During Bovine Early Embryonic Development1