Expression data from fetal hepatocytes from control or Cnot3KO E16.5 embryos treated with Actinomycin D for 0, 6 or 12h

mRNA degradation critically contributes to liver development and function. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify abnormally stabilized mRNAs in the fetal hepatocytes lacking Cnot3, a core subunit of the CCR4-NOT complex. Liver-specific Cnot3 knockout (Cnot3LKO) mice were generated by expressing Cre recombinase under the control of Albumin promoter. Fetal hepatocytes were prepared from embryos after crossing control or Cnot3LKO mice. Total RNAs were prepared before or after Actinomycin D treatment and used for hybridization on Affymetrix microarrays.