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Fig.S7 (related to Figs. 5 and 6). KDM3A facilitates the chromatin binding of Neurog2. (A, B) Anti-H3K9me2 ChIP-qPCR analyses indicating that overexpression of wild type 6MT-KDM3A (1 ng) but not a catalytic mutant 6MT-KDM3A (H1130Y, 1 ng) reduced the expression levels of H3K9me2 on the promoter regions of neurod1 (A) and tubb2b (B). (C, D) Anti-H3K27ac ChIP-qPCR analyses indicating that ectopic 6MT-KDM3A or a catalytic mutant 6MT-KDM3A (H1130Y) did not alter the H3K27ac marks on the promoter regions of neurod1 (C) or tubb2b (D). (E) Anti-H3K9me2ChIP-qPCR analyses showing 3A MO (80 ng) increased the H3K9me2 marks on the promoter region of tubb2b. (F) Anti-Myc ChIP-qPCR analyses indicating that 80 ng 3A MO but not cMO blocked the overexpressed 6MT-Neurog2 from accessing the promoter of tubb2b.

Image published in: Lin H et al. (2017)

Copyright © 2017. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License.

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