petition between remodelers. Dr. Workman A-83-01 focused the last part of his talk on the role of enoki mushroom, the fly homolog of the human monocytic leukemia zinc finger protein, YBF2, something about silencing-2, TAT-interactive protein 60 acetyltransferase. Enok is expressed at high levels in embryos and localized to spire and mael in oocytes. Moreover, Enok acetylates H3K23 in flies, playing a crucial role in oogenesis. Colyn Crane-Robinson began his lecture by discussing his laboratory’s initial undertaking: generating specific antibodies against acetylated histone residues. After performing ChIP experiments using antiAcH4 and anti-AcH2A.Z antibodies, Dr. Crane-Robinson’s team could confirm that both histone modifications frequently co-habit the same nucleosomes. Moreover, by using ChIP-Seq experiments they were able to show that AcH2A.Z is present at both active and poised transcription start signal, at enhancers and at insulators. He proposed the concept of H2A. Z, typically acetylated, as a general facilitator of nucleosome remodeling that allows access to chromatin by a wide variety of activating and repressing complexes.6 Lorraine Pillus described some aspects of MYST family proteins. KAT5 lysine acetyltransferase 5 is the human homolog of acetyltransferase in yeast. Both enzymes are essential for cell viability, and genomic aberration of Tip60 is found in human carcinomas. Dr. Pillus presented that it is possible to rescue the phenotype of of esa1D cells by deletion of SDS3, which encodes a non-catalytic subunit of the reduced potassium depending 3 large deacetylase complex.7 Furthermore, she 
reported that a new mark, H2A-pY57, is critical in casein kinase 2 mediated transcriptional elongation which helps explain why earlier studies found the H2A-Y57A PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19840835 mutation to be lethal. The H2A-Y57F mutants affect histone modifications involved in transcriptional regulation. Jean-Marc Victor explained a physical view of the correlation between transcriptional activity and histone modifications through a mechanistic and spatial structure explanation based on allostery. The allostery in DNA and protein interactions can play an important role in gene regulation. He showed how the chromatin fiber provides a proof of principle for this model. The anchoring mode of DNA is controlled by the acetylation of H3, determining a clamped mode when the H3 tail is de-acetylated or, in contrast, a free hinged mode when it is acetylated. The spatial structure of chromatin determined by the acetylation of the tails of histones also determines the affinity of proteins that bind to DNA, thus modulating gene expression. Astrid Hagelkruys examined the impact of HDAC1 and HDAC2 isoformspecific functions in the development of the brain and epidermis. The deletion of 3 of the 4 HDAC1/HDAC2 alleles has a different phenotype, depending on the remaining allele and the organ affected. In the brain, normal development occurs when only one allele of HDAC2 is remaining, whereas mice with a single allele of HDAC1 die shortly after birth. In contrast, mice with a single allele of HDAC1 in the epidermis have a normal epidermal development, but when only one allele of HDAC2 has expressed spontaneous papiloma formation and hyperkeratosis is observed. www.tandfonline.com Epigenetics 447 Protein kinase C, which is a direct target of HDAC2, is an important regulator of cell death, cell cycle progression, and energy metabolism, and its inhibition rescues the differentiation phenotypes
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