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BSDB-BSCB Meeting Report Part I

Posted by , on 12 June 2010

The recent joint meeting of the British Societies for Developmental Biology (BSDB) and Cell Biology (BSCB) in Warwick provided an exciting opportunity to catch a glimpse of the future of these two fields. “Old” questions of how cell fates are allocated during development are now being tackled with new technologies and new knowledge of how gene expression can be regulated.

Since I made the decision to write this report after the conference was over, I’m outlining only a few talks which I have attended and found interesting. I’ve written this in three parts. Part one covers some of the presentations on transcriptional regulation, the second part will be about transcription factor networks, and part number three covers several topics which do not fit into the first two categories: Stem cells, limb development and evo-devo.

Part 1: Transcriptional Regulation

Mike Levine (University of California, USA) opened the conference by presenting his lab’s work on the suppression of transcriptional noise during dorsal-ventral patterning of the early Drosophila embryo. One mechanism they have found to underly such robustness is the deployment of multiple enhancers for the same expression patterns, so-called “shadow enhancers”. Levine also reported that rapid transcriptional responses to signals can involve a mechanism in which RNA polymerase II is kept in a paused state near the promoter, ready to receive a ‘go’ signal. It remains to be seen if these mechanisms are utilized in other systems to confer robustness and responsiveness.

To map the location, density and orientation of paused RNA polymerase II (Pol II), John Lis (Cornell University, USA) introduced a recently developed method called “GRO (Genome-wide nuclear Run-On) -seq”, which uses nuclear run-on followed by large-scale parallel sequencing. The analysis of these parameters in mouse embryonic stem (ES) cells and isogenic embryonic fibroblasts (MEFs) uncovered peaks of paused Pol II on both the sense and antisense strands close to the transcription start site in CpG-associated promoters. Lis pointed out that the function of the antisense polymerase remains unclear, but it presumably acts by regulating transcription orientation and efficiency. He also explained why the presence of paused polymerase is interesting for us developmental biologists: The comparison of the Pol II profiles in ES cells and MEFs revealed that many genes differ in their Pol II state in the two cell types.

Bob Kingston (Harvard Medical School, USA) discussed how Polycomb Group (PcG) genes are involved in regulating the changes in Hox gene expression during differentiation of human ES cells. They identified a region between HOXD11 and HOXD12 (“D11.12”), which is H3K27 methylated, occupied by PcG proteins, and shows changes in nucleosome occupancy upon differentiation. Such an arrangement is characteristic of Drosophila Polycomb response elements (PREs), cis-regulatory sequences required for PcG mediated repression. In a series of experiments they could show that specific sequences in this region are required for PcG-mediated repressive activity of a D11.12 reporter, and that this repression was maintained during differention, thereby identifying the first PRE-like element in a mammalian system. Furthermore, the endogenous D11.12 locus is dynamically occupied by PcG proteins in differentiating hESCs. Whether or not this region is required for embryonic development remains to be determined.

Peter Fraser (The Babraham Institute, Cambridge, UK) showed us what transcriptional regulation looks like in the nucleus: He presented his team’s work on intra- and interchromosomal interactions during transcription. In mouse erythroid cells, they encountered sub-nuclear foci highly enriched in active RNA Pol II, so-called “Pol II factories”. Transcriptionally active genes up-regulated by the transcription factor Klf1 in the definitive erythroid lineage, were predominantly present in the same foci, together with large amounts of Klf1 protein. They found that Klf1 is required for this clustering of co-regulated genes. Fraser’s work encourages us to refrain from thinking of transcriptional regulation as a linear phenomenon, but we should rather start imagining the process in its 3-dimensional spatial, nuclear context, in which specific transcription factories cluster regulatory proteins and their co-regulated targets, to optimize the coordination of transcriptional control. These factories preferentially transcribe a specific network of genes and might be a major factor underlying tissue-specific chromosome organization.

More about the discussion of transcription factor networks as it took place in this meeting will follow in part two.




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