Hormone-controlled changes in the differentiation state of post-mitotic neurons

While we think of neurons as having a fixed identity, many show spectacular plasticity.(1-10) Metamorphosis drives massive changes in the fly brain;(11,12) neurons that persist into adulthood often change in response to the steroid hormone ecdysone.(13,14) Besides driving remodeling,(11-14) ecdysone signaling can also alter the differentiation status of neurons.(7,15 )The three sequentially born subtypes of mushroom body (MB) Kenyon cells (gamma, followed by alpha'/beta', and finally alpha/beta)(16 )serve as a model of temporal fating.(17-21) gamma neurons are also used as a model of remodeling during metamorphosis. As gamma neurons are the only functional Kenyon cells in the larval brain, they serve the function of all three adult subtypes. Correspondingly, larval gamma neurons have a similar morphology to alpha'/beta' and alpha/beta neurons-their axons project dorsally and medially. During metamorphosis, gamma neurons remodel to form a single medial projection. Both temporal fate changes and defects in remodeling therefore alter gamma-neuron morphology in similar ways. Mamo, a broad-complex, tramtrack, and bric-a-brac/poxvirus and zinc finger (BTB/POZ) transcription factor critical for temporal specification of alpha'/beta' neurons,(18,19) was recently described as essential for gamma remodeling. In-22 a previous study, we noticed a change in the number of adult Kenyon cells expressing gamma-specific markers when mamo was manipulated.(18) These data implied a role for Mamo in gamma-neuron fate specification, yet mamo is not expressed in gamma neurons until pupariation,(18,22) well past gamma specification. This indicates that mamo has a later role in ensuring that gamma neurons express the correct Kenyon cell subtype-specific genes in the adult brain.