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. 2019 Aug 26;33(11):12541–12553. doi: 10.1096/fj.201901213R

Figure 8.

Figure 8

Injection of Hdac1 cRNA successfully restored the level of Trp53 acetylation in Sin3a-depleted embryos. A) Immunostaining analyses of Trp53K379 in morulae. The signal intensity of Trp53K79 in Sin3a-deficient embryos was restored in response to Hdac1 cRNA injection (KD+Hdac1 vs. KD+Cas9; 5–10 embryos per group; n = 3. Scale bar, 25 μm). B) Quantification of the signal intensity for the experiment in A. C) Hdac1 was mutated at the deacetylase site and mRNA was produced in vitro. Wild-type Hdac1 (WT) and mutant Hdac1 (MT) was introduced into zygotes, and 2-cell embryos were collected for immunocytochemical analysis. Hdac1 expression induced up-regulation of Sin3a regardless of the deacetylase activity of Hdac1.