Skip to main content
. Author manuscript; available in PMC: 2010 Jun 11.
Published in final edited form as: Neuron. 2009 Jun 11;62(5):641–654. doi: 10.1016/j.neuron.2009.04.025

Figure 8. Transcriptionally active chromatin is established by RA and CBP in MNe.

Figure 8

(A) The histone modifications in MNe upon RA treatment were analyzed by ChIP assays in P19 cells expressing Ngn2. RA facilitates histone H3/H4-acetylation and H3-lysine-4-trimethylation (H3K4me3), while suppressing H3-lysine-9-diemthylation (H3K9me2), in MNe. (B, C) ChIP assays using the spinal cord dissected from mutant embryos of genotypes shown in the boxes. Histone H3-acetylation (B) and H3K4me3 (C) in MNe are impaired in CBP-inactivated E12.5 embryonic spinal cord. (D) The working model. Ngn2 and RAR form a complex in pMN progenitors. The extrinsic signal RA binds RAR and facilitates the association of a chromatin modifier CBP with the Ngn2/RAR-complex. Assembly of the Ngn2/RAR/CBP-complex on Ngn2-target motor neuron enhancers triggers their transcriptionally active open chromatin structure marked by H3/4-acetylation and results in subsequent motor neuron gene expressions, leading to the differentiation to motor neurons.