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Fluorescent proteins can report on many cellular variables. Here, authors develop a method for reporting high local densities, and use it to show that density distribution of heterochromatin in mouse embryonic stem cells are not in a liquid phase.

Two commonly prescribed drugs, statins and aminobisphosphonates, may be helpful in combating the rare aging disorder, Hutchinson-Gilford progeria syndrome (pages 767–772).

The authors show that DNA methylation patterns in one tissue can inform on those in another, under certain conditions, and devise an algorithm that allows identification of differential DNA methylation. They applied it to an archaic human dataset, revealing information about human brain evolution in the absence of preserved brain tissue.

Stem-cell differentiation is controlled by RNA processing — as well as by gene expression and transcription. This finding is a milestone towards realizing these cells' potential for research and therapy. See Letter p.241

Progerin, a mutated form of lamin A, causes the premature ageing disease Hutchinson-Gilford progeria syndrome and is also involved in normal ageing. Progerin accumulation leads to distinct chromatin-related defects and the NURD complex appears to affect ageing-related chromatin defects.

Reprogramming of somatic cells is an inherently inefficient process. A new study has now identified histone H3K36 methylation as a crucial reprogramming barrier that operates downstream of TGFβ signalling. Global inhibition of H3K36 methylation induced PRC2-dependent silencing of mesenchymal genes and dramatically increased reprogramming efficiency.

The role of RNA splicing in the regulation of stem cell properties has remained largely unexplored. The splicing-associated protein SON is now shown to be necessary for embryonic stem cell maintenance, by influencing the splicing of pluripotency regulators.

There is increasing evidence that an 'open' chromatin state contributes to maintenance of pluripotency in stem cells, and that this requires regulation of both the global chromatin state and local repression of transcription. This regulation may also be relevant for chromatin control during reprogramming or during tumorigenesis.

How traits specific to modern humans have evolved is difficult to study. Here, Gokhman et al. compare measured and reconstructed DNA methylation maps of present-day humans, archaic humans and chimpanzees and find that genes that affect vocal tract and facial anatomy show methylation changes between archaic and modern humans.

In mammals, two major non-centromeric histone H3 (H3.1/2 and H3.3) variants, display distinct nuclear distribution patterns across the genome and use distinct deposition pathways. Here the authors reveal insights on the nuclear distribution of H3.1 and H3.3 variants, focusing on their relative enrichment at chromocenters throughout the cell cycle and in different cellular states.

Bivalent chromatin domains contain opposing histone modifications that assist cell lineage specification. Two studies report a role for Dppa2 and Dppa4 in the establishment of bivalency and the prevention of de novo DNA methylation at development-related genes in mouse embryonic stem cells.

Chromatin in embryonic stem cells is present in an open state presumably to facilitate gene expression changes required for pluripotency and subsequent multilineage differentiation. This study describes roles for lamin A, histone acetylation and G9a-mediated histone H3 lysine 9 methylation in regulating chromatin plasticity in these cells.

We know that most splicing reactions take place co-transcriptionally, but how the transcription machinery facilitate splicing of introns is unknown. Here the authors show that the 5′ splice site remains associated with the transcription machinery during intron synthesis through U1 snRNP, providing a basis for the rapid splicing reaction of introns.

Genetic imprinting ensures monoallelic gene expression critical for normal embryonic development. Here the authors take advantage of human haploid parthenogenic embryonic stem cells lacking paternal alleles to identify, by genome-wide screening, factors involved in the regulation of imprinted genes.

The chromatin remodelling proteins Snf2h and Snf2l regulate nucleosome spacing. Here, the authors show that Snf2hablation impairs chromatin organization of neuronal lineages during mouse embryonic and post-natal cerebellar development.

A hallmark of stem cells is an open chromatin largely devoid of heterochromatin, but which molecules are required to maintain it is unknown, as well as whether an open chromatin is necessary for the differentiation potential of stem cells. Here, the chromatin remodelling factor Chd1 is shown to be required to maintain the open chromatin state of pluripotent mouse embryonic stem cells and to be essential for the pluripotency of these cells.

What makes a stem cell is still poorly understood. Recent studies have uncovered that chromatin might hold some of the keys to how embryonic stem cells maintain their pluripotency, their ability to self-renew and induce lineage specification.

A comprehensive metagenomic analysis of chromatin immunoprecipitation–sequencing and microarray analysis (ChIP-seq and ChIP-chip) data from mouse embryonic stem cells provides insight into how histone gene transcription is controlled. The work reveals a complex mode of regulation, with multiple factors acting to regulate transcription of core and linker histones.

Splicing and transcription have been argued to be coupled, but the mechanisms behind this are unclear. Published data sets examining nucleosome positioning are now analyzed and show that exons tend to have higher nucleosome occupancy than introns. This may indicate why metazoan exons are ∼150 nucleotides, similar to the length of DNA on a nucleosome.