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Meeting report: 11th EMBL conference on transcription and chromatin - August 23–26, 2014 Heidelberg, Germany Sascha H C Duttke To cite this article: Sascha H C Duttke (2014) Meeting report: 11th EMBL conference on transcription and chromatin - August 23–26, 2014 - Heidelberg, Germany, Epigenetics, 9:10, 1317-1321, DOI: 10.4161/15592294.2014.967590 To link to this article: http://dx.doi.org/10.4161/15592294.2014.967590

Accepted author version posted online: 30 Oct 2014.

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MEETING REPORT Epigenetics 9:10, 1317--1321; October 2014; © 2014 Taylor & Francis Group, LLC

Meeting report: 11th EMBL conference on transcription and chromatin - August 23–26, 2014 - Heidelberg, Germany Sascha H C Duttke* Section of Molecular Biology; University of California; San Diego, CA USA

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Keywords: chromatin, DNA methylation, EMBL, enhancers, Heidelberg, heterochromatin divergent transcription, histone modifications, stem cells, topologically associating domains (TAD), transcription, TRF2

An all-star lineup of presenters and a friendly scientific atmosphere contributed to make the 11th EMBL Conference on Transcription and Chromatin (August 23–26, 2014) once again a meeting to remember. Scientist from over 30 countries met in Heidelberg, Germany to share their latest insights in transcription and chromatin research. DNA methylation, topologically associating domains, polycomb proteins, enhancers, divergent transcription, and the effect of chromatin and its modifications on gene expression were among the central topics. The overall high quality and the extent of novel material included in the presentations made summarizing this conference in a meeting report format a remarkably enjoyable challenge. I apologize in advance to those speakers whose excellent work was not to included due to space constraints.

DNA Methylation and Reprogramming Henk Stunnenberg (University of Nijmegen) kicked off this year’s meeting with the latest insights in DNA methylation and its role in stem cell reprogramming. Mouse embryonic stem cells (ESCs) grown in the presence of inhibitors of MEK and GSK3 (2i media) are in ground state and globally hypomethylated compared to those grown in serum (primed state).1 Stunnenberg’s laboratory utilized this system to investigate the mechanisms and kinetics of DNA methylation occurring when ESCs are moved from serum to 2i media. Whereas expression of TET1, TET2, and DNMT1 is similar under both growing conditions, DNMT3a/b and DNMT3L are downregulated 4 to 32-fold in 2i-grown cells. Demethylation occurs over several days but could be accelerated by supplementing vitamin C. An increase in global 5hmC levels pointed to the involvement of a TET-mediated demethylation mechanism. Kinetic analyses suggested a switch from fast, TETdependent demethylation to a passive mechanism. Notably, the kinetics varied between different genomic regions. In the absence of TET1/2, vitamin C did not increase DNA demethylation. Surprisingly, TET1/2 were dispensable for ESC dedifferentiation from primed to ground state. It could thus be speculated that *Correspondence to: Sascha Duttke; Email: [email protected] Submitted: 09/15/2014; Accepted: 09/15/2014 http://dx.doi.org/10.4161/15592294.2014.967590


DNA methylation may not play an essential role in ESC reprogramming when cells are switched from serum to 2i media.

Topologically Associating Domains and Regulatory Landscapes Digits and genitals share many developmental properties. Denis Duboule (EPFL and University of Geneva) showed that the regulatory landscapes and topologically associating domains (TADs) of genitals and digits largely overlap. Digits and genitals share many common enhancers that facilitate the spatiotemporal expression of the HoxD genes. However, a few key regions facilitated genital or digit specific gene expression. This observation suggests that regulatory landscapes may be fertile ground to evolve novel enhancers. Innovations likely occur within genomic niches, defined by TADs, that could have facilitated the evolution of pleiotropic loci. This further exemplifies the evolutionary co-option of Hox genes at multiple sites.

DNA Localization Matters The nuclear periphery is occupied by inactive or poorly transcribed genes and enriched for chromatin marks associated with gene repression. This organization can change during differentiation raising the question of whether loss of transcription targets chromatin to the nuclear periphery or vice versa. Wendy Bickmore (MRC Human Genetics, Edinburgh) utilized fluorescent probes in combination with synthetic transcription activators targeting genes at the nuclear periphery in mouse embryonic stem cells to reveal that chromatin remodeling events direct positioning of transcriptionally active DNA away from the nuclear periphery. Together, these observations suggest that chromatin modification may guide the nuclear organization of the genome.

Polycomb and GlcNAc In Drosophila, O-GlcNAcylation (GlcNAc), which is mediated by O-GlcNAc transferase (Ogt), co-localizes with Polycomb proteins at Polycomb Response Elements (PRE) genome-wide. J€ urg Muller’s group (Max-Planck Institute of Biochemistry, Martinsried) further investigated the role of GlcNAc in Polycomb-



mediated gene repression. They found that Polycomb complex 1 (PRC1) subunit Ph is O-GlcNAcylated; however, PRC1 is still bound to PRE in the absence of Ogt. Further analysis showed that Ph aggregates in the absence of GlcNAc, both in vivo and in vitro. Their studies suggest a role for GlcNAc in controlling the formation of ordered Ph assemblies, which, in turn, may facilitate the interaction between distantly bound PRC1 complexes to repress gene transcription.

boundary between active and inactive chromatin between Hoxa5 and Hoxa6 in motor neuron cells to address this question. Hoxa5 and Hoxa6 are separated by a CTCF binding site. Deletion of this binding site reduced CTCF occupancy of adjacent sites and, most notably, caused the active, H3K4me3marked domain to expand and the repressive, H3K27me3marked domain to shrink. CTCF demarcated distinct topological and chromatin domains and thus functions as a bona fide insulator.

Enhancers, Promoters, and Divergent Transcription

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Diverse Roles for Histone Modifications Around 1000 enhancers regulate a few hundred genes that dictate patterning of the early Drosophila embryo. Mike Levine (UC Berkeley) visualized nascent even-skipped RNA expression by addition of MS2 RNA stem loops, which had been fluorescently labeled with GFP. This revealed a connection between mitosis and embryonic patterning. Notably, even-skipped expression exhibits bursts of transcription, and refinement of its expression pattern has been linked to transcriptional repression during mitosis.2 In the example of hunchback, a shadow enhancer improves the spatial and temporal precision of gene activation. Transcriptional bursts may be important for the dynamic regulation of segmentation genes expression and, possibly, other gene regulatory networks. In differentiated cells, most enhancers and their chromatin signatures are already established. How this chromatin signatures are established, however, is not well understood. Minna Kaikkonen (University of Eastern Finland) utilized Kdo2-lipid A (KLA) stimulus of macrophages to study the de novo formation of about 3000 enhancers. Transcription at enhancers predates the deposition of H3K4me1/2, a hallmark of enhancers, and correlates with H3K4me1/2 signatures genome-wide.3 Mixed lineage leukemia proteins (MLLs) mediate the deposition of H3K4me1/2 in a transcription dependent process. These data highlight the importance of transcription in enhancer formation. John Lis (Cornell University, Ithaca, NY) utilized global run-on sequencing followed by 5’ cap enrichment (GRO-cap) to differentially analyze stable and unstable transcripts in human cells. Unstable transcripts were enriched at enhancers as well as upstream and antisense to annotated promoters. The level of transcription at enhancers correlated with the level of histone modifications at those enhancers. Notably, promoters and enhancers showed similar patterns of divergent transcription start sites (TSSs), nucleosome positioning, and transcription factor localization. Up to 63% of unstable transcripts could be explained by the presence of polyadenylation and termination sequences. Together, these data provide another example of the close similarity between enhancers and promoters.

Establishing Chromatin Boundaries How are chromatin domain boundaries formed? Danny Reinberg (NYU, School of Medicine, NY, NY) looked at the


Histone modifications are known transcriptional regulators. Tony Kouzarides (Gurdon Institute, University of Cambridge) expanded this view by presenting several novel modifications with distinct functions. PADI4-mediated citrullination of a histone H1 arginine (R) residue located close to H1 DNA binding site resulted in H1 displacement and subsequent chromatin decondensation.4 In this way, PADI4, which is found in neutrophils and pluripotent stem cells, regulates the opening up of higher order chromatin. Another novel modification he discussed was the methylation of glutamine (Q) in histone H2A (Q105 in yeast and Q104 in human), which is mediated by Nop1 or fibrillarin, respectively.5 Notably, this modification is constrained to the 35S rDNA transcriptional unit and, thus, represents the first identified modification to be limited to genes transcribed by a specific RNA polymerase, namely RNA polymerase I. Kouzarides further demonstrated a role for histone methylation in the regulation of DNA replication. Trimethylation of histone H3 lysine 36 (H3K36) in yeast is mediated by Set2 and commonly associated with actively transcribed promoters. H3K36me1, however, is enriched at DNA replication sites. Kouzarides group found that H3K36me1 positively regulates the binding of the DNA replication licensing factor MCM2 in Sphase, while the adjacent H3K37me1 antagonized the process. Mutation of K37 to alanine (A), which phenocopies K37me1, caused a delay in the G1 to S transition and decreased the binding affinity of the whole MCM complex. H3K36me1, but not H3K36me3, was mediated by Set4. No modifying enzyme for H3K37 is yet known. These data also suggest a role for histone modifications in the regulation of the cellular switch from transcription to DNA replication, which do not occur simultaneously.

Transcription in the Absence of Active Chromatin Marks Silvia Perez (Center for Genomic Regulation, Barcelona) utilized available modENCODE data to investigate the histone marks of regulated genes during Drosophila development. Intriguingly, regulated genes lacked histone marks typically associated with active transcription, such as H3K4me3, H3K9ac, or H3K27ac, which are usually present


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at promoters of stably expressed genes. The same results could be observed when looking at tissue-specific genes in less heterogeneous tissues, such as imaginal discs of 3rd instar larvae. Sequencing of nascent RNA demonstrated that genes lacking active histone marks were indeed actively transcribed. Regulated and tissue-specific genes were mainly classified as black chromatin, previously described by Filion et al. as repressed chromatin void of many histone marks; however, in this case, the genes were re-expressed at even higher levels.6 The current model proposes that active transcription facilitates the establishment of chromatin marks, which, in turn, facilitate downstream events. Nevertheless, these genes do not display active marks despite being actively transcribed.

Heterochromatin Formation Tightly packed heterochromatin is associated with gene repression. Gunnar Schotta (LMU, Munich) utilized a GFP reporter driven by a retrotransposon promoter containing a short heterochromatin induction sequence (SHIN) that recruits Setdb1-dependent silencing through trimethylation of H3K9. This enabled a shRNA screen that identified a thalassemia/mental retardation syndrome X-linked (ATRX) as a regulator, silencing transposons of the intracisternal A particle (IAP) family. ATRX localization to IAP elements is required for timely silencing. ATRX interacts with the death domain associated protein DAXX, which promotes heterochromatin formation, independently of H3.3. Knockout of ATRX did not alter chromatin structure on a global scale but increased microccocal nuclease accessibility at retrotransposons. This observation suggests that ATRX, together with DAXX, is important for the fast establishment and robust maintenance of heterochromatin. About one third of all human sequence-specific transcription factors encode for KRAB-containing zinc finger proteins, which repress transcription through heterochromatin formation. Didier Trono (EPFL, Lausanne) found that KRAB and its cofactor KAP1 repress long interspersed element-1 (LINE1) transposons. KAP1 knockdown induced the expression of evolutionary more ancient LINE-1 elements, while more recent versions of LINE-1 were unaffected. Zinc fingers are highly diverse in their ability to recognize DNA sequences. However, for KRAB to evolve into recognizing newer LINE1 element requires time, opening up the question of how more recent LINE-1 elements are silenced. Interestingly, Trono showed that silencing of more recently evolved LINE1 elements is dependent on sRNA-guided DNA methylation, highlighting DNA methylation as the immediate early mechanism for LINE-1 silencing. Thus, in the same way that diverse antibodies recognize different proteins, diverse KRABs police the genome and silence distinct LINE-1 elements, thereby promoting genomic stability. This arms race may explain why about one third of all sequence specific transcription factors encode for KRABs.


Higher Order Chromatin Transcription The wrapping of DNA around a core histone octamer forms an 11 nm fiber that folds into a transcriptionally repressed higher-order chromatin structure upon addition of linker histone H1. In biochemical studies of higher order chromatin activation, Robert Roeder (Rockefeller University, New York, NY) showed that the H1 chaperone NAP1 is directly recruited by activator-bound p300. This, in turn, leads to core histone acetylation by p300, loss of NAP1, H1, and H2A/H2B, and chromatin decompaction. The subsequent loss of H3/H4 is facilitated by recruitment of an ATP-dependent remodeler such as ACF. The necessity of core histone acetylation for these processes was established by mutation of histone acetylation sites. Thus, NAP1 recruitment plays a key role in higher-order chromatin decompaction and subsequent transcription.

Transcription and Nucleosomes DNA is tightly wrapped around nucleosomes, which form a natural barrier for RNA polymerase II (RNAP II) and are mobilized in the process of transcription. Steven Henikoff’s group (Hutchinson Cancer Research Center, Seattle, WA) utilized a combination of trimethylpsoralen-seq, which measures genome-wide supercoiling, and CATCH-IT, which captures nucleosome eviction, and identified torsion as a driver of nucleosome turnover. Negative supercoiling stabilizes the nucleosome, while positive supercoiling destabilizes it.7 The entry site of C1 nucleosome provided the major barrier for RNAP II. Notably, these data differ from previous in vitro results that suggested that the barrier was closer to the nucleosome dyad axis. The barrier strength was reduced in the presence of H2AZ, which also reduced RNAP II stalling.8 In the genome, nucleosome positions are arranged in a specific pattern along a gene. Frank Pugh (Penn State University, PA) argued that some positioning information is encoded in the DNA sequence, particularly for the nucleosome-free promoter region, but the information is insufficient for periodic positioning of the nucleosomes. Addition of whole cell yeast nuclear extract and ATP to the histone-DNA mixture allows reconstructing of the nucleosome array patterning.9 To investigate the importance of the different chromatin remodeling enzymes in nucleosome positioning, the Pugh and Korber’s groups generated extracts from yeast lacking a given remodeler and then added it back to characterize its function in nucleosome array formation. They also examined purified remodelers and sequence-specific general regulatory factors. They showed RSC to be involved in clearing out the nucleosome-free region of the promoter, while ISW1a and ISW2 together were able to position the nucleosome array in the absence of transcription or DNA replication. Thus, combinations of remodelers and sequence-specific factors are sufficient to generate well-positioned arrays akin to what is seen in vivo.



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CTD Modifications and Divergent Transcription The RNAP II C-terminal domain (CTD) is a tandem repeat of 7 aminoacids (Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7) undergoing posttranslational modifications that are important for gene regulation. Phosphorylation of Tyr1 in yeast associates with RNAP II in the gene body and impairs recruitment of the termination factor during transcriptional elongation.10 JeanChristophe Andrau (CNRS, Montpellier) reported that, in mammals, mutation of Tyr1 results in CTD degradation, which is lethal. In human cells, Tyr1P associates with the leading edge of RNAP II at promoters with antisense paused transcripts and at actively transcribed enhancers that lack Ser2P.11 These findings highlight differential functions for CTD modification between yeast and mammals.

Christoph M€ uller (EMBL, Heidelberg) presented the structures of RNAP I and III. RNAP I contains 14 subunits including 2 TFIIF-like subunits, while RNAP III contains 17 subunits including 2 TFIIF as well as 3 TFIIE-like subunits. Yeast RNAP I crystal structure was solved at 3 A .16 The RNAP I DNA binding cleft is larger than in RNAP II and contains an extended loop that mimics the DNA backbone in the cleft. Interestingly, the RNAP I structure can be very nicely fitted in the cryo-EM reconstitution of RNAP III, determined earlier by the M€ uller lab at 10 A resolution.17 These structural studies provide further insights into the overall conservation of the architecture between RNA polymerases.

Regulation of the Endogenous Circadian Rhythm Basal Transcription The TATA box binding protein (TBP) is part of RNAP I, II, and III transcription initiation complexes and highly conserved among humans and archaea. Alongside TBP, negative regulators NC2 and Mot1p were found to localize to highly transcribed promoters. Marc Timmers (University Medical Center Utrecht) now showed that these proteins function in the repression of TATA-mediated cryptic transcription from TATA-like sequences in the gene body that become exposed during transcription.12 Tamar Juven-Gershon (Bar-Ilan University, Ramat Gan) identified the TATA box binding protein related factor 2 (TRF2), as an essential factor for the transcription of core promoters that depend on the DPE core promoter motif. Furthermore, using a microfluidic system of mechanically induced trapping of molecular interactions (MITOMI), her group showed that TRF2-containing complexes preferentially bind Inr and DPE-containing promoters.13 TRF2 was previously reported to be essential for the transcription of Drosophila ribosomal protein genes in TCT motif-dependent core promoters.14 Together, these results propose the existence of multiple, distinct TBP- or TRF2-dependent RNAP II transcription systems.15

Most vital processes in animals are subjected to daily rhythms, controlled by an endogenous circadian timing system consisting of a master pacemaker in the brain’s suprachiasmatic nucleus and circadian clocks in virtually all body cells. Ueli Schibler (University of Geneva) used real time monitoring of circadian luciferase reporter gene expression in peripheral organs to better understand the multiple direct and indirect pathways that synchronize the “clocks” in our body. Studies in mice suggest that feeding times are the predominant cue for the internal rhythm. Transgenic mice without circadian liver clocks helped discover temperature-sensitive heat shock genes and cold-inducible RNA-binding proteins as additional cues. The circadian rhythm of cultured NIH3T3 cells could be synchronized through simulated body temperature rhythms, which notably regulated gene expression through the rhythmic activity of heat shock transcription factor 1 (HSF1) and the splicing efficiency of the mRNA encoding CIRP, a cold-inducible RNA-binding protein. At 33 C, most CIRP pre-mRNA is spliced correctly; however, at 38 C, the transcripts are preferentially degraded. Together, these observations suggest that not only food uptake and metabolism but also temperature provide key cues for setting the phase of oscillating gene expression in peripheral organs.

Structural Studies of RNAP I, RNAP III, and RNAP II Preinitiation Complex with Mediator The minimal transcription initiation complex required for the transcription of TATA-dependent RNAP II core promoters consists of TBP, TFIIB, TFIIF, and RNAP II. Patrick Cramer (Gene Center and Max-Planck-Institute for Biophysical Chemistry, G€ottingen) presented the cryo-EM structure of this core pre initiation complex at 7.8 A , which further enabled the reconstruction of the complex from crystal structures. Addition of Mediator to this core transcription complex (9.7 A ) showed the Mediator head module to stabilize the complex by contacting TFIIB and facilitating CTD phosphorylation by the TFIID kinase.


Outlook The 11th EMBL Conference on Transcription and Chromatin once again impressed with an excellent line-up of speakers, well-organized execution, and an outstanding environment. Not surprisingly, this ever-growing meeting18 attracted over 450 scientists, most of which are already looking forward to attending the 12th installment of this meeting in August 2016.

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.


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I apologize for the limited selection of presentations due to format restrictions. I would like to thank Carolina Garcia Sabate (EMBL) for administrative help, Epigenie (http://epigenie.com) for covering the conference fee and the UCSD Graduate School of Biological Sciences and James T. Kadonaga for support. I am also grateful to all cited authors and Dr. Barbara Rattner, for their help editing this manuscript.

SD is the recipient of the University of California, San Diego Molecular Biology/Cancer Center Fellowship, a Ruth Newmark Fellow, and supported by National Institutes of Health grant R01GM041249 to James T. Kadonaga.

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Meeting report: 11th EMBL conference on transcription and chromatin - August 23-26, 2014 - Heidelberg, Germany.

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