ArticleDevelopment (Cambridge, England)2016
Notch maintains Drosophila type II neuroblasts by suppressing expression of the Fez transcription factor Earmuff.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Electron transport chain complex I and mitochondrial fusion regulate ROS for differentiation in Drosophila neural stem cells.Stem cell reports · 2026Article
- N-myristoyl Transferase Maintains Type II Neuroblasts through Notch Signaling in Drosophila.Neuroscience bulletin · 2026Article
- Spen and Nito prevent dedifferentiation of intermediate progenitors by maintaining Notch target expression in stem cells at low levels.Cell reports · 2026Article
- Altering cell size asymmetry inbioRxiv : the preprint server for biology · 2025Article
- Article
- Seven-up acts in neuroblasts to specify adult central complex neuron identity and initiate neuroblast decommissioning.Development (Cambridge, England) · 2024Article
- Article
- Seven-up acts in neuroblasts to specify adult central complex neuron identity and initiate neuroblast decommissioning.bioRxiv : the preprint server for biology · 2023Article
- Evolutionary dynamics of genome size and content during the adaptive radiation of Heliconiini butterflies.Nature communications · 2023Article
- Single cell RNA-seq analysis reveals temporally-regulated and quiescence-regulated gene expression in Drosophila larval neuroblasts.Neural development · 2022Article
- Mitochondrial fusion regulates proliferation and differentiation in the type II neuroblast lineage in Drosophila.PLoS genetics · 2022Article
- The Ets protein Pointed P1 represses Asense expression in type II neuroblasts by activating Tailless.PLoS genetics · 2022Article
- Enhancer analysis of the Drosophila zinc finger transcription factor Earmuff by gene targeting.Hereditas · 2021Article
- Homeodomain protein Six4 prevents the generation of supernumerary Drosophila type II neuroblasts and premature differentiation of intermediate neural progenitors.PLoS genetics · 2021Article
- Insect Transcription Factors: A Landscape of Their Structures and Biological Functions inInternational journal of molecular sciences · 2018Review
- Article
- bHLH-O proteins balance the self-renewal and differentiation of Drosophila neural stem cells by regulating Earmuff expression.Developmental biology · 2017Article
- Asymmetric Notch Amplification to Secure Stem Cell Identity.Developmental cell · 2017Article
- An Hdac1/Rpd3-Poised Circuit Balances Continual Self-Renewal and Rapid Restriction of Developmental Potential during Asymmetric Stem Cell Division.Developmental cell · 2017Article
- Failure of the PTEN/aPKC/Lgl Axis Primes Formation of Adult Brain Tumours inBioMed research international · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Notch signaling is crucial for maintaining neural stem cell (NSC) self-renewal and heterogeneity; however, the underlying mechanism is not well understood. In Drosophila, loss of Notch prematurely terminates the self-renewal of larval type II neuroblasts (NBs, the Drosophila NSCs) and transforms type II NBs into type I NBs. Here, we demonstrate that Notch maintains type II NBs by suppressing the activation of earmuff (erm) by Pointed P1 (PntP1). We show that loss of Notch or components of its canonical pathway leads to PntP1-dependent ectopic Erm expression in type II NBs. Knockdown of Erm significantly rescues the loss-of-Notch phenotypes, and misexpression of Erm phenocopies the loss of Notch. Ectopically expressed Erm promotes the transformation of type II NBs into type I NBs by inhibiting PntP1 function and expression in type II NBs. Our work not only elucidates a key mechanism of Notch-mediated maintenance of type II NB self-renewal and identity, but also reveals a novel function of Erm.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.