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Summary cis-regulatory changes play a central role in morphological divergence, yet the regulatory principles underlying emergence of human traits remain poorly understood. Here, we use epigenomic profiling from human and chimpanzee cranial neural crest cells to systematically and quantitatively annotate divergence of craniofacial cis-regulatory landscapes. Epigenomic divergence is often attributable to genetic variation within TF motifs at orthologous enhancers, with a novel motif being most predictive of activity biases. We explore properties of this cis-regulatory change, revealing the role of particular retroelements, uncovering broad clusters of species-biased enhancers near genes associated with human facial variation, and demonstrating that cis-regulatory divergence is linked to quantitative expression differences of crucial neural crest regulators. Our work provides a wealth of candidates for future evolutionary studies and demonstrates the value of "cellular anthropology," a strategy of using in-vitro-derived embryonic cell types to elucidate both fundamental and evolving mechanisms underlying morphological variation in higher primates.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2007.09.026 Byline: Tomek Swigut (1), Joanna Wysocka (1) Abstract: Methylation of lysine 27 on histone H3 (H3K27me) by the Polycomb complex (PRC2) proteins is associated with gene silencing in many developmental processes. A cluster of recent papers () identify the JmjC-domain proteins UTX and JMJD3 as H3K27-specific demethylases that remove this methyl mark, enabling the activation of genes involved in animal body patterning and the inflammatory response. Author Affiliation: (1) Department of Chemical and Systems Biology and Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA

A study revealed that LSD1, a nuclear amine oxidase homolog, is a bona fide histone H3 lysine 4 demethylase. Results suggest that LSD1's specificity and activity is in fact regulated by associated protein cofactors.

A common component of MLL1, MLL2, and hSet1 human proteins H3 K4 methyltransferase complexes, the WD40-repeat protein WDR5, directly associates with histone H3 di- and trimethylated at K4 and with H3-K4-dimethlylated nucleosomes is demonstrated. Results show that a WD40-repeat protein acts as a modification and suggest a mechanism for reading and writing an epigenetic mark for gene activation.

A stable complex containing MLL1 and MOF proteins is immunoaffinity purified from a human cell line that stably expresses an epitope-tagged WDR5 subunit. Results indicate an activator-based mechanism for joint MLL1 and MOF recruitment and targeted methylation and acetylation along with a molecular explanation for the closely correlated distribution of Histone-H3 lysine-K4 methylation and H4 K16 acetylation on active genes.

Research has been conducted on the asymmetric cell division. The experiments with the SHORT-ROOT gene that encodes a putative transcription factor with homology to SCARECROW are discussed.

The cell lineages of the Arabidopsis root meristem are generated when the initial cells undergo asymmetric division. However, mutations such as the scarecrow (SCR) could disrupt the asymmetric division that generates the cortex and endodermis, resulting in roots that are missing one cell layer. A study shows that SCR plays a major role in regulating the root's radial organization.