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      Epigenetic (re)programming of caste-specific behavior in the ant Camponotus floridanus

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          Abstract

          Eusocial insects organize themselves into behavioral castes whose regulation has been proposed to involve epigenetic processes, including histone modification. In the carpenter ant Camponotus floridanus, morphologically distinct worker castes called minors and majors exhibit pronounced differences in foraging and scouting behaviors. We found that these behaviors are regulated by histone acetylation likely catalyzed by the conserved acetyltransferase CBP. Transcriptome and chromatin analysis in brains of scouting minors fed pharmacological inhibitors of CBP and histone deacetylases (HDACs) revealed hundreds of genes linked to hyperacetylated regions targeted by CBP. Majors rarely forage, but injection of a HDAC inhibitor or small interfering RNAs against the HDAC Rpd3 into young major brains induced and sustained foraging in a CBP-dependent manner. Our results suggest that behavioral plasticity in animals may be regulated in an epigenetic manner via histone modification.

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          Distinct roles of GCN5/PCAF-mediated H3K9ac and CBP/p300-mediated H3K18/27ac in nuclear receptor transactivation.

          Qihuang Jin, Li-Rong Yu, Lifeng Wang … (2011)
          Histone acetyltransferases (HATs) GCN5 and PCAF (GCN5/PCAF) and CBP and p300 (CBP/p300) are transcription co-activators. However, how these two distinct families of HATs regulate gene activation remains unclear. Here, we show deletion of GCN5/PCAF in cells specifically and dramatically reduces acetylation on histone H3K9 (H3K9ac) while deletion of CBP/p300 specifically and dramatically reduces acetylations on H3K18 and H3K27 (H3K18/27ac). A ligand for nuclear receptor (NR) PPARδ induces sequential enrichment of H3K18/27ac, RNA polymerase II (Pol II) and H3K9ac on PPARδ target gene Angptl4 promoter, which correlates with a robust Angptl4 expression. Inhibiting transcription elongation blocks ligand-induced H3K9ac, but not H3K18/27ac, on the Angptl4 promoter. Finally, we show GCN5/PCAF and GCN5/PCAF-mediated H3K9ac correlate with, but are surprisingly dispensable for, NR target gene activation. In contrast, CBP/p300 and their HAT activities are essential for ligand-induced Pol II recruitment on, and activation of, NR target genes. These results highlight the substrate and site specificities of HATs in cells, demonstrate the distinct roles of GCN5/PCAF- and CBP/p300-mediated histone acetylations in gene activation, and suggest an important role of CBP/p300-mediated H3K18/27ac in NR-dependent transcription.
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            Recovery of learning and memory is associated with chromatin remodelling.

            André Fischer, Farahnaz Sananbenesi, Xinyu Wang … (2007)
            Neurodegenerative diseases of the central nervous system are often associated with impaired learning and memory, eventually leading to dementia. An important aspect in pre-clinical research is the exploration of strategies to re-establish learning ability and access to long-term memories. By using a mouse model that allows temporally and spatially restricted induction of neuronal loss, we show here that environmental enrichment reinstated learning behaviour and re-established access to long-term memories after significant brain atrophy and neuronal loss had already occurred. Environmental enrichment correlated with chromatin modifications (increased histone-tail acetylation). Moreover, increased histone acetylation by inhibitors of histone deacetylases induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories. These data suggest that inhibition of histone deacetylases might be a suitable therapeutic avenue for neurodegenerative diseases associated with learning and memory impairment, and raises the possibility of recovery of long-term memories in patients with dementia.
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              Virtual ligand screening of the p300/CBP histone acetyltransferase: identification of a selective small molecule inhibitor.

              Erin M. Bowers, Gai Yan, Chandrani Mukherjee … (2010)
              The histone acetyltransferase (HAT) p300/CBP is a transcriptional coactivator implicated in many gene regulatory pathways and protein acetylation events. Although p300 inhibitors have been reported, a potent, selective, and readily available active-site-directed small molecule inhibitor is not yet known. Here we use a structure-based, in silico screening approach to identify a commercially available pyrazolone-containing small molecule p300 HAT inhibitor, C646. C646 is a competitive p300 inhibitor with a K(i) of 400 nM and is selective versus other acetyltransferases. Studies on site-directed p300 HAT mutants and synthetic modifications of C646 confirm the importance of predicted interactions in conferring potency. Inhibition of histone acetylation and cell growth by C646 in cells validate its utility as a pharmacologic probe and suggest that p300/CBP HAT is a worthy anticancer target. 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 0404511
                Journal ID (pubmed-jr-id): 7473
                Journal ID (nlm-ta): Science
                Journal ID (iso-abbrev): Science
                Title: Science (New York, N.Y.)
                ISSN (Print): 0036-8075
                ISSN (Electronic): 1095-9203
                Publication date Nihms-submitted: 16 September 2016
                Publication date (Print): 1 January 2016
                Publication date PMC-release: 11 October 2016
                Volume: 351
                Issue: 6268
                Page: aac6633
                Affiliations
                [1 ]Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA
                [2 ]Program in Epigenetics, University of Pennsylvania, Philadelphia, PA 19104, USA
                [3 ]Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
                [4 ]School of Life Sciences, Arizona State University, Tempe, AZ 85287, USA
                [5 ]Department of Biology, New York University, New York, NY 10003, USA
                [6 ]Department of Entomology, University of California, Riverside, CA 92521, USA
                [7 ]Department of Biological Sciences, Vanderbilt University, Nashville, TN 37232, USA
                [8 ]Department of Molecular Pharmacology and Biochemistry, New York University School of Medicine, New York, NY 10016, USA
                [9 ]Department of Genetics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA
                Author notes
                Article
                Accession ID: PMC5057185 Pmcid ID: PMC5057185 Pmc-uid ID: 5057185 Manuscript ID: nihpa817047
                DOI: 10.1126/science.aac6633
                PMC ID: 5057185
                PubMed ID: 26722000
                SO-VID: 6df4f2bc-1aec-40b3-91d8-c621e476dc59
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