@article {6303,
	title = {The bHLH repressor Deadpan regulates the self-renewal and specification of Drosophila larval neural stem cells independently of Notch.},
	journal = {PLoS One},
	volume = {7},
	year = {2012},
	month = {2012 Oct 8},
	pages = {e46724},
	abstract = {<p>Neural stem cells (NSCs) are able to self-renew while giving rise to neurons and glia that comprise a functional nervous system. However, how NSC self-renewal is maintained is not well understood. Using the Drosophila larval NSCs called neuroblasts (NBs) as a model, we demonstrate that the Hairy and Enhancer-of-Split (Hes) family protein Deadpan (Dpn) plays important roles in NB self-renewal and specification. The loss of Dpn leads to the premature loss of NBs and truncated NB lineages, a process likely mediated by the homeobox protein Prospero (Pros). Conversely, ectopic/over-expression of Dpn promotes ectopic self-renewing divisions and maintains NB self-renewal into adulthood. In type II NBs, which generate transit amplifying intermediate neural progenitors (INPs) like mammalian NSCs, the loss of Dpn results in ectopic expression of type I NB markers Asense (Ase) and Pros before these type II NBs are lost at early larval stages. Our results also show that knockdown of Notch leads to ectopic Ase expression in type II NBs and the premature loss of type II NBs. Significantly, dpn expression is unchanged in these transformed NBs. Furthermore, the loss of Dpn does not inhibit the over-proliferation of type II NBs and immature INPs caused by over-expression of activated Notch. Our data suggest that Dpn plays important roles in maintaining NB self-renewal and specification of type II NBs in larval brains and that Dpn and Notch function independently in regulating type II NB proliferation and specification.</p>
},
	keywords = {Animals, Basic Helix-Loop-Helix Transcription Factors, Drosophila, Drosophila Proteins, Larva, Neural Stem Cells, Notch, Nuclear Proteins, Receptors},
	issn = {1932-6203},
	doi = {10.1371/journal.pone.0046724},
	author = {Zhu, Sijun and Wildonger, Jill and Barshow, Suzanne and Younger, Susan and Huang, Yaling and Lee, Tzumin}
}
@article {792,
	title = {Gradients of the Drosophila Chinmo BTB-zinc finger protein govern neuronal temporal identity.},
	journal = {Cell},
	volume = {127},
	year = {2006},
	month = {2006 Oct 20},
	pages = {409-22},
	abstract = {<p>Many neural progenitors, including Drosophila mushroom body (MB) and projection neuron (PN) neuroblasts, sequentially give rise to different subtypes of neurons throughout development. We identified a novel BTB-zinc finger protein, named Chinmo (Chronologically inappropriate morphogenesis), that governs neuronal temporal identity during postembryonic development of the Drosophila brain. In both MB and PN lineages, loss of Chinmo autonomously causes early-born neurons to adopt the fates of late-born neurons from the same lineages. Interestingly, primarily due to a posttranscriptional control, MB neurons born at early developmental stages contain more abundant Chinmo than their later-born siblings. Further, the temporal identity of MB progeny can be transformed toward earlier or later fates by reducing or increasing Chinmo levels, respectively. Taken together, we suggest that a temporal gradient of Chinmo (Chinmo(high) {\textendash}\&gt; Chinmo(low)) helps specify distinct birth order-dependent cell fates in an extended neuronal lineage.</p>
},
	keywords = {5{\textquoteright} Untranslated Regions, Amino Acid Sequence, Animals, Brain, Cell Differentiation, Cell Lineage, Developmental, Drosophila, Drosophila Proteins, Gene Expression Regulation, Larva, Molecular Sequence Data, Morphogenesis, Mushroom Bodies, Mutation, Nerve Tissue Proteins, Neurons, Post-Translational, Protein Processing, Time Factors, Transgenes, Zinc Fingers},
	issn = {0092-8674},
	doi = {10.1016/j.cell.2006.08.045},
	author = {Zhu, Sijun and Lin, Suewei and Kao, Chih-Fei and Awasaki, Takeshi and Chiang, Ann-Shyn and Lee, Tzumin}
}
