Ian Duncan

During animal development, a small number of intercellular signals are responsible for almost all patterning.  These signals are used over and over, controlling different sets of target genes at different times and in different tissues.  How are changes in target gene specificity achieved?  In large part, such changes are controlled temporally, with global shifts in responsiveness occurring as development proceeds from one stage of the life cycle to the next.  Our research goal is to understand the mechanisms by which such global temporal changes in target gene competence are directed.

Our focus is on metamorphosis, a time at which dramatic changes in target gene responsiveness facilitate the patterning of adult structures from their larval precursors.  We have identified the transcription factor E93 as a key determinant of these changes in competence.  E93 is expressed only during metamorphosis, when it is induced by the molting hormone ecdysone, and is required for many or all pupa-specific patterning processes.  In a detailed study of one such process, we showed that E93 causes a shift in the competence of the Distal-less gene to respond to epidermal growth factor signaling.  The broad requirement for E93 in pupal development suggests that E93 functions to control responsiveness at many other loci.  We are currently working to determine how broadly E93 functions within the genome, the mechanisms by which E93 alters responsiveness of Distal-less, and the potential role of E93 in the evolution of metamorphosis.