Developing a global understanding of the PRC and NuRD complexes in stem cell differentiation and in disease


In this article Stevens et al. illustrate how the determination of single-cell genome structure provides a new approach for investigating biological processes.

In this paper Chittock et al. discuss some highlights of recent PcG structures and the insights they have given us into how these complexes regulate transcription through chromatin.

In this publication Pascual et al. show that metastasis-initiating cells particularly rely on dietary lipids to promote metastasis.

In this paper Mas and Di Croce outline novel insights and perspectives regarding the function of Polycomb complexes in shaping the stem cell genome architecture, and discuss how this function might be required to properly orchestrate transcriptional programs during differentiation.

In this article Beringer et al. show, that Elongin BC is recruited to chromatin by the PRC2-associated factor EPOP (Elongin BC and Polycomb Repressive Complex 2 Associated Protein). Both EPOP and Elongin BC are required to maintain low levels of expression at PRC2 genomic targets. The results indicate that keeping the balance between activating and repressive cues is a more general feature of chromatin in pluripotent stem cells than previously appreciated.

In this paper Koehler et al. present a baculovirus-based protein engineering method that enables site-specific introduction of unique functionalities in a eukaryotic protein complex recombinantly produced in insect cells.

In this paper Spruijt et al. show that ZMYND8 bridges NuRD to a number of putative DNA-binding zinc finger proteins. The MYND domain of ZMYND8 directly interacts with PPPLΦ motifs in the NuRD subunit GATAD2A.

In this paper Rinaldi et al. show that in human epidermal stem cells, the two proteins Dnmt3a and Dnmt3b bind in a histone H3K36me3-dependent manner to the most active enhancers and are required to produce their associated enhancer RNAs.

Comet et al. propose in this article that the opposing roles of PRC2 in cancer are a consequence of the molecular function of the complex in maintaining, rather than specifying, the transcriptional repression state of its several thousand target genes.

In this paper Lindeboom et al. used matched exome and transcriptome data from 9,769 human tumors to systematically elucidate the rules of NMD targeting in human cells.

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