Animal Culture: Chimpanzee Table Manners?

(Figure 1A,B). These results illustrate that DCC distribution is dynamically specified by developmental changes in gene expression. The aspect of transcriptional activity recognized by the DCC is unknown. Possibilities include chromatin features (e.g., nucleosome-free regions or variants and modifications of histones), or the transcription machinery itself. One suspect is histone H3 K4 methylation, a ubiquitous mark of active promoters. C. elegans DPY-30 is homologous to a subunit of the conserved COMPASS complex that establishes H3 K4 methylation, and DPY-30 is required both for normal levels of this modification and for localization of some DCC subunits to the X chromosome (reviewed in [6]). The most puzzling aspect of transcription-dependent DCC spreading is its purpose. The observation that more DCC tends to bind more highly expressed promoters suggests that it acts locally, repressing individual genes in proportion to their degree of transcription. But contradictory to that model, a genome-wide analysis of gene expression in dosage compensation mutants found little correlation between genes that undergo dosage compensation and those that have DCC bound to their promoters [12]. Moreover, Ercan et al. [2] did not detect repression of autosomal genes into which the DCC had spread on X;A fusions. A remaining enigma is why DCC localization is tuned to underlying transcription state and yet, by gene expression profiling, the DCC does not seem to directly regulate transcription of genes at which it localizes. Perhaps spreading generates a sufficient number and distribution of DCC sites to achieve a global reconfiguration of chromosome architecture, analogous to condensin action during mitosis. Alternatively, like mammalian X inactivation or Polycomb repression of Hox genes, the DCC could relocate the X into a repressive nuclear compartment [3,7,15]. Condensin facilitates the nuclear clustering and silencing of tRNA loci in Saccharomyces cerevisiae, suggesting it could play such a role [16]. In multiple examples of domain-wide gene regulation, evolution has converged on a common strategy of sequence-specific recruitment and sequence-independent spreading [1]. An advantage of this strategy is that specificity need only be conferred to a small number of DNA sequences and recruitment proteins. General spreading can subsequently propagate regulation over an entire domain. The reports covered here have significantly advanced our understanding of one such system. These studies also raise new questions about how the transcription-influenced localization of the C. elegans DCC along the X relates to its function in dosage compensation. Elucidating this mechanism is a major challenge for the future.