Epigenetics and the control of multicellularity

Abstract

The Cantoblanco Workshop on Chromatin at the Nexus of Cell Division and Differentiation took place between 30 June and 2 July 2008, in Cantoblanco, Madrid, Spain, and was organized by U. Grossniklaus, C. Gutierrez and B. Scheres. ![][1] See Glossary for abbreviations used in this article At many points during development and adult life, cells have to react to regulatory cues, and decide between self‐renewal and entering terminal differentiation. To do so, they integrate many inputs from their environment and their own developmental programme. This workshop aimed to explore the role of chromatin and epigenetics in the coordinated regulation of cell division and differentiation. The conference gathered researchers from various fields of epigenetics who work with different model systems, including yeast, Drosophila , vertebrates and Arabidopsis thaliana . They presented mostly unpublished results on a wide range of epigenetic mechanisms that are involved in the control of proliferation and differentiation, highlighting many fundamental roles of the chromatin components in these processes; this made for a truly exciting scientific programme. Several adult stem‐cell systems have been identified in Drosophila , providing exceptionally favourable models for the analysis of the dynamic self‐renewal of short‐lived terminally differentiated cell types. B. Edgar (Seattle, WA, USA) showed that transiently ablated enterocysts induce intestinal stem‐cell (ISC) proliferation after the expression of the caspase activator Reaper or the JNK activator Hemipterous, resulting in rapid intestinal regeneration. The data support a homeostatic feedback control between enterocysts and ISCs through the JAK/STAT and JNK signalling pathways. By using a Pseudomonas entomophila infection model, Edgar found that, besides NOTCH, JAK/STAT and JNK, the EGFR signalling pathway also controls ISC proliferation; this indicated that the ISC niche is also partly provided by progeny enterocysts ensuring the homeostatic control of ISC proliferation in response to stress, injury or infections. M. Fuller (Stanford, CA, … [1]: /embed/graphic-1.gif