It is becoming increasingly evident that both vertebrate and invertebrate neural progenitor cells exhibit programmed temporal changes in their competence to generate specific neuronal cell types, but how is this competency controlled? Two articles in this issue address this question by studying Drosophila neuroblast lineage progression.

On p. 657, Michael Cleary and co-workers investigate the role of Polycomb repressor complexes (PRCs) in regulating neuroblast competence. In the Drosophila neuroblast 7-1 (NB7-1) lineage, the transcription factor Kruppel (Kr) specifies the third-born U3 motoneuron, but competence to generate U3 cells is limited to early divisions and is gradually lost when the neuroblasts transition to making interneurons. The researchers show that PRC loss of function extends the ability of Kr to induce U3 fate, whereas PRC gain of function causes precocious loss of competence to make motoneurons. The analysis of other neuroblast lineages that undergo a motoneuron-to-interneuron production transition demonstrates that PRCs also act to restrict motoneuron competence in these lineages. The researchers thus propose a model in which PRCs act to set up motoneuron-specific windows of competence in various neuroblasts that transition from motoneuron-to-interneuron production.

On p. 678, Stefan Thor and colleagues focus on the Drosophila embryonic neuroblast NB5-6T lineage to investigate how cell proliferation and cell fate specification are integrated during development. NB5-6T neuroblasts give rise to a lineage of 20 cells, including a differentiated set of neurons that are born at the very end of the lineage and that express Apterous: the Ap neurons. The authors identify two independent factors, Prospero and Notch, that act in concert to control the proliferation of NB5-6T daughter cells as the lineage progresses temporally; Prospero controls daughter cell proliferation in the early lineage and Notch activity then limits daughter cell proliferation in the late lineage, when Ap neurons are generated directly from neuroblasts, resulting in a programmed differentiation switch. Thus, the authors conclude, the control of neuronal daughter cell proliferation is integrated with temporal progression to ensure that the correct numbers of each unique cell type are generated.