2 Matching Annotations
  1. Jul 2018
    1. On 2015 Nov 04, Carl de Boer commented:

      After publication, we found that our proposed mechanism was unclear, so we have published on figshare [1] a detailed model describing how a poly-dA:dT can be asymmetrically read by chromatin remodelers (http://dx.doi.org/10.6084/m9.figshare.1515926). Further, motivated by recent work by the Kornberg group, which showed that RSC can further decrease the nucleosome occupancy at poly-dA:dT sites [2], and unpublished results from Frank Pugh’s group [3], we checked for enrichment of chromatin modifiers surrounding poly-dA:dT tracts. RSC was specifically enriched in the 5’ offset NFR relative to the poly-dA:dT (http://dx.doi.org/10.6084/m9.figshare.1515927) [4], consistent with RSC recognizing and becoming stalled specifically at poly-dA:dT sequences in a strand-specific manner.

      [1] de Boer, C; Hughes, TR (2015): Model for how poly-dA:dT sites act as nucleosome turnstiles. figshare. http://dx.doi.org/10.6084/m9.figshare.1515926 Retrieved 18:47, Aug 28, 2015 (GMT)

      [2] Lorch Y, Maier-Davis B, Kornberg RD. Role of DNA sequence in chromatin remodeling and the formation of nucleosome-free regions. Genes Dev. 2014 Nov 15;28(22):2492-7. doi: 10.1101/gad.250704.114.

      [3] Wal M, Krietenstein N, Watanabe S, Peterson CL, Korber P, Pugh BF. Unpublished results.

      [4] de Boer, C; Hughes, TR (2015): The RSC complex may be the poly-A nucleosome turnstile mechanism. figshare. http://dx.doi.org/10.6084/m9.figshare.1515927 Retrieved 18:47, Aug 28, 2015 (GMT)


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.

  2. Feb 2018
    1. On 2015 Nov 04, Carl de Boer commented:

      After publication, we found that our proposed mechanism was unclear, so we have published on figshare [1] a detailed model describing how a poly-dA:dT can be asymmetrically read by chromatin remodelers (http://dx.doi.org/10.6084/m9.figshare.1515926). Further, motivated by recent work by the Kornberg group, which showed that RSC can further decrease the nucleosome occupancy at poly-dA:dT sites [2], and unpublished results from Frank Pugh’s group [3], we checked for enrichment of chromatin modifiers surrounding poly-dA:dT tracts. RSC was specifically enriched in the 5’ offset NFR relative to the poly-dA:dT (http://dx.doi.org/10.6084/m9.figshare.1515927) [4], consistent with RSC recognizing and becoming stalled specifically at poly-dA:dT sequences in a strand-specific manner.

      [1] de Boer, C; Hughes, TR (2015): Model for how poly-dA:dT sites act as nucleosome turnstiles. figshare. http://dx.doi.org/10.6084/m9.figshare.1515926 Retrieved 18:47, Aug 28, 2015 (GMT)

      [2] Lorch Y, Maier-Davis B, Kornberg RD. Role of DNA sequence in chromatin remodeling and the formation of nucleosome-free regions. Genes Dev. 2014 Nov 15;28(22):2492-7. doi: 10.1101/gad.250704.114.

      [3] Wal M, Krietenstein N, Watanabe S, Peterson CL, Korber P, Pugh BF. Unpublished results.

      [4] de Boer, C; Hughes, TR (2015): The RSC complex may be the poly-A nucleosome turnstile mechanism. figshare. http://dx.doi.org/10.6084/m9.figshare.1515927 Retrieved 18:47, Aug 28, 2015 (GMT)


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.