The control of organ number is vital to the proper development of an organism. For example, the decision to make two lungs but just one heart allows vertebrate body to function correctly. My work is focused on understanding how this type of decision is made in Drosophila –in particular; I am interested in understanding how each eye-antennal disc produces a single adult antenna. I have uncovered a role for the Trithorax Group (TrxG) of epigenetic regulators in this decision. Reductions in some members of the TrxG result in an adult fly with four antennae instead of the normal two. In other cases, this antennal duplication requires the simultaneous reduction of a TrxG member and twin of eyeless (toy), a selector gene for eye fate and the Drosophila homolog of vertebrate Pax6. Data from our lab also shows that eliminating toy and a second Pax6 gene, eyeless (ey), during certain developmental windows causes identical antennal duplications. These results demonstrate novel roles for Pax6 in antennal development and for TrxG proteins in regulating organ number. There is precedent for communication between Pax proteins and TrxG members. It has been reported that vertebrate Pax2 physically interacts with PTIP (Pax Transcriptional Activation Domain Interacting Protein), a TrxG protein. To uncover how Pax6 and TrxG cooperate to control antennal numbers we are using candidate gene approach beginning with the Wingless (Wg) pathway. Prior studies have shown that some TrxG members regulate Wg signaling and that reductions in early Wg expression within the antennal field can lead to its duplication. In addition to its role in antennal development, Wg signaling is also necessary for preventing the initiation of ectopic furrows. We have observed ectopic furrows in discs with reduced levels of TrxG. Our model suggests that Pax6 and TrxG cooperate to regulate Wg signaling in the eye and early antennal discs. Disrupting this regulatory circuit results in ectopic furrows and an increase in the number of the antennal segments.