Fig. 6

HDAC4 suppressed c-Kit expression via deacetylation. The binding of PLZF and HDAC4 (A), β-catenin and PLZF (B) were determined in SPCs using co-IP. The inhibitory effect of PLZF and HDAC4 on c-Kit (C) and Stra8 (D) was evaluated in dual-luciferase assay (1. pGL-c-Kit + pcDNA3.1, 2. pGL-c-Kit + pcDNA3.1-Plzf, 3. pGL-c-Kit + pcDNA3.1-Hdac4, 4. pGL-c-Kit + pcDNA3.1-Plzf + pcDNA3.1-Hdac4; 5. pGL-Stra8 + pcDNA3.1, 6. pGL-Stra8 + pcDNA3.1-Plzf, 7. pGL-Stra8 + pcDNA3.1-Hdac4, 8. pGL-Stra8 + pcDNA3.1-Plzf + pcDNA3.1-Hdac4), n=3. Acetylation lysine IP coupled with Western blot was used to detect the impact of HDAC4 on c-Kit acetylation (E). A schematic illustration described the regulatory mechanism that HDAC4 could directly bind to c-Kit to suppress its expression via deacetylation (F). The regulatory pattern of cadherins on SPCs fate was schematically summarized (G). Data represent as mean ± SD *p < 0.05; **p < 0.01