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. 2010 Sep 23;6(9):e1001132. doi: 10.1371/journal.pgen.1001132

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Xu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) Growth and developmental defects of the dcaf26^KO strain were complemented by wild-type Myc-DCAF26 or mutated Myc-DCAF26R976A, but not Myc-DCAF26dWD3. (B) Loss of DNA methylation in dcaf26^KO was rescued by expressing Myc-DCAF26 or Myc-DCAF26R976A, but not Myc-DCAF26dWD3. (C) Loss of H3K9 trimethylation at the ψ63 region in the dcaf26^KO strain was rescued by expressing Myc-DCAF26 or Myc-DCAF26R976A, but not Myc-DCAF26dWD3. (D) Western blot analysis showing that the loss of global H3K9 trimethylation in dcaf26^KO was restored by Myc-DCAF26 or Myc-DCAF26R976A, but not Myc-DCAF26dWD3. H3 antibody was used as the positive control and as the control for integrity of the nucleosome structure.