The acquisition of competence is a key mechanism for refining global signals to distinct spatial and temporal responses. The molecular basis of competence, however, remains poorly understood. Here, we show that the beta FTZ-F1 orphan nuclear receptor functions as a competence factor for stage-specific responses to the steroid hormone ecdysone during Drosophila metamorphosis. beta FTZ-F1 mutants pupariate normally in response to the late larval pulse of ecdysone but display defects in stage-specific responses to the subsequent ecdysone pulse in prepupae. The ecdysone-triggered genetic hierarchy that directs these developmental responses is severely attenuated in beta FTZ-F1 mutants, although ecdysone receptor expression is unaffected. This study define beta FTZ-F1 as an essential competence factor for stage-specific responses to a steroid signal and implicates interplay among nuclear receptors as a mechanism for achieving hormonal competence.

The generation of cellular diversity is essential in embryogenesis, especially in the central nervous system. During neurogenesis, cell interactions or asymmetric protein localization during mitosis can generate daughter cells with different fates. Here we describe the asymmetric localization of a messenger RNA and an RNA-binding protein that creates molecular and developmental differences between Drosophila neural precursors (neuroblasts) and their daughter cells, ganglion mother cells (GMCs). The prospero (pros) mRNA and the RNA-binding protein Staufen (Stau) are asymmetrically localized in mitotic neuroblasts and are specifically partitioned into the GMC, as is Pros protein. Stau is required for localization of pros RNA but not of Pros protein. Loss of localization of Stau or of pros RNA alters GMC development, but only in embryos with reduced levels of Pros protein, suggesting that pros RNA and Pros protein act redundantly to specify GMC fate. We also find that GMCs do not transcribe the pros gene, showing that inheritance of pros RNA and/or Pros protein from the neuroblast is essential for GMC specification.

Drosophila is an ideal system for identifying genes that control central nervous system (CNS) development. Particularly useful tools include molecular markers for subsets of neural precursors (neuroblasts) and the simple expression pattern of the even-skipped (eve) gene in a subset of neurons. Here we provide additional molecular markers for identified neuroblasts, including several with near single cell specificity. In addition, we use these new markers to trace the development of several eve+ neurons. Our results shows that the eve+ aCC/pCC neurons develop from a different neuroblast than previously thought, and have led us to assign new names for several neuroblasts. These results are supported by DiI cell lineage analysis of neuroblasts identified in vivo.