Abstract
Intermediate neural progenitor cells (INPs) need to avoid differentiation and cell cycle exit while maintaining restricted developmental potential, but mechanisms preventing differentiation and cell cycle exit of INPs are not well understood. In this study, we report that the Drosophila homolog of mammalian Sp8 transcription factor Buttonhead (Btd) prevents premature differentiation and cell cycle exit of INPs in Drosophila larval type II neuroblast (NB) lineages. We show that the loss of Btd leads to elimination of mature INPs due to premature differentiation of INPs into terminally dividing ganglion mother cells. We provide evidence to demonstrate that Btd prevents the premature differentiation by suppressing the expression of the homeodomain protein Prospero in immature INPs. We further show that Btd functions cooperatively with the Ets transcription factor Pointed P1 to promote the generation of INPs. Thus, our work reveals a critical mechanism that prevents premature differentiation and cell cycle exit of Drosophila INPs.
Highlights
Intermediate neural progenitor cells (INPs) play a critical role in increasing the brain size and complexity
RNAi knockdown of Btd using the type II NB lineage-specific pntP1-GAL4 (Zhu et al, 2011) as a driver led to a complete elimination of mature INPs in about 50% of type II NB lineages (Figure 1B–B′,G–H)
To determine if the reduction/loss of Pointed P1 (PntP1) is responsible for the ectopic Ase expression and/or the loss of INPs in btd mutant type II NB lineages, we examined if restoring PntP1 expression was sufficient to suppress ectopic Ase expression and/or rescue the loss of INPs resulting from the loss of Btd by expressing UAS-pntP1 in btd mutant type II NB clones
Summary
Intermediate neural progenitor cells (INPs) play a critical role in increasing the brain size and complexity. Recent studies in developing human brains as well as other mammalian brains suggest that an expansion of the number of transiently amplifying INPs, the outer sub-ventricular zone radial glia-like cells (oRGs), likely contributes to the increased cortical size and complexity in humans and other gyrencephalic animals (Fietz et al, 2010; Hansen et al, 2010; Lui et al, 2011; Wang et al, 2011). The recently discovered type II neuroblasts (NBs, the Drosophila NSCs) in developing Drosophila larval brains provide an excellent model system for studying mechanisms regulating the generation and proliferation of INPs (Bello et al, 2008; Boone and Doe, 2008; Bowman et al, 2008).
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