1. Centre for Molecular Biology Heidelberg (ZMBH), University of Heidelberg, 69120 Heidelberg, Germany
2. †Present address: The National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK

Correspondence to: Renato Paro¹ Correspondence and requests for materials should be addressed to R.P. (Email: paro@zmbh.uni-heidelberg.de).

Abstract

During the regeneration of Drosophila imaginal discs, cellular identities can switch fate in a process known as transdetermination¹. For leg-to-wing transdetermination, the underlying mechanism involves morphogens such as Wingless that, when activated outside their normal context, induce ectopic expression of the wing-specific selector gene vestigial^{2, 3}. Polycomb group (PcG) proteins maintain cellular fates by controlling the expression patterns of homeotic genes and other developmental regulators⁴. Here we report that transdetermination events are coupled to PcG regulation. We show that the frequency of transdetermination is enhanced in PcG mutant flies. Downregulation of PcG function, as monitored by the reactivation of a silent PcG-regulated reporter gene, is observed in transdetermined cells. This downregulation is directly controlled by theJun amino-terminal kinase (JNK) signalling pathway, which is activated in cells undergoing regeneration. Accordingly, transdetermination frequency is reduced in a JNK mutant background. This regulatory interaction also occurs in mammalian cells, indicating that the role of this signalling cascade in remodelling cellular fates may be conserved.

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