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Resolving Heart Regeneration by Replacement Histone Profiling.

Developmental cell (2017-03-02)
Joseph Aaron Goldman, Guray Kuzu, Nutishia Lee, Jaclyn Karasik, Matthew Gemberling, Matthew J Foglia, Ravi Karra, Amy L Dickson, Fei Sun, Michael Y Tolstorukov, Kenneth D Poss
RESUMEN

Chromatin regulation is a principal mechanism governing animal development, yet it is unclear to what extent structural changes in chromatin underlie tissue regeneration. Non-mammalian vertebrates such as zebrafish activate cardiomyocyte (CM) division after tissue damage to regenerate lost heart muscle. Here, we generated transgenic zebrafish expressing a biotinylatable H3.3 histone variant in CMs and derived cell-type-specific profiles of histone replacement. We identified an emerging program of putative enhancers that revise H3.3 occupancy during regeneration, overlaid upon a genome-wide reduction of H3.3 from promoters. In transgenic reporter lines, H3.3-enriched elements directed gene expression in subpopulations of CMs. Other elements increased H3.3 enrichment and displayed enhancer activity in settings of injury- and/or Neuregulin1-elicited CM proliferation. Dozens of consensus sequence motifs containing predicted transcription factor binding sites were enriched in genomic regions with regeneration-responsive H3.3 occupancy. Thus, cell-type-specific regulatory programs of tissue regeneration can be revealed by genome-wide H3.3 profiling.

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Sigma-Aldrich
ANTI-FLAG® M2 monoclonal antibody produced in mouse, 1 mg/mL, clone M2, affinity isolated antibody, buffered aqueous solution (50% glycerol, 10 mM sodium phosphate, and 150 mM NaCl, pH 7.4)
Sigma-Aldrich
ChIPAb+ Histona H3.3 - Conjunto de cebador y anticuerpo validado para ChIP, from rabbit, purified by affinity chromatography