ArticleDevelopment (Cambridge, England)2014
Brain tumor specifies intermediate progenitor cell identity by attenuating β-catenin/Armadillo activity.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- The RNA-binding activity of theRNA biology · 2026Article
- Orb2 RNA-binding activity promotes neural stem cell development and brain growth in Drosophila larvae.Cell reports · 2026Article
- Temporal neuronal differentiation programs safeguard neuronal diversity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- RNA-binding is the essential biological function of thebioRxiv : the preprint server for biology · 2026Article
- The CPEB ortholog Orb2 regulates brain size through the TRIM-NHL RNA-binding protein, Brain tumor.bioRxiv : the preprint server for biology · 2025Article
- mRNA decay pre-complex assembly drives timely cell-state transitions during differentiation.Cell reports · 2025Article
- The TRIM-NHL RNA-binding protein Brain Tumor coordinately regulates expression of the glycolytic pathway and vacuolar ATPase complex.Nucleic acids research · 2024Article
- CNN-based glioma detection in MRI: A deep learning approach.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024Article
- Ribogenesis boosts controlled by HEATR1-MYC interplay promote transition into brain tumour growth.EMBO reports · 2024Article
- Regenerative growth is constrained by brain tumor to ensure proper patterning in Drosophila.PLoS genetics · 2023Article
- Article
- Premature translation of the Drosophila zygotic genome activator Zelda is not sufficient to precociously activate gene expression.G3 (Bethesda, Md.) · 2022Article
- The Ets protein Pointed P1 represses Asense expression in type II neuroblasts by activating Tailless.PLoS genetics · 2022Article
- Regulation of Neural Stem Cell Competency and Commitment during Indirect Neurogenesis.International journal of molecular sciences · 2021Review
- Molecular and biological functions of TRIM-NHL RNA-binding proteins.Wiley interdisciplinary reviews. RNA · 2021Review
- Article
- Multilayered gene control drives timely exit from the stem cell state in uncommitted progenitors duringGenes & development · 2018Article
- A Novel Mutation in Brain Tumor Causes Both Neural Over-Proliferation and Neurodegeneration in AdultG3 (Bethesda, Md.) · 2018Article
- Brain Tumor promotes axon growth across the midline through interactions with the microtubule stabilizing protein Apc2.PLoS genetics · 2018Article
- Article
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Authors and funding
4 authors.
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Abstract
During asymmetric stem cell division, both the daughter stem cell and the presumptive intermediate progenitor cell inherit cytoplasm from their parental stem cell. Thus, proper specification of intermediate progenitor cell identity requires an efficient mechanism to rapidly extinguish the activity of self-renewal factors, but the mechanisms remain unknown in most stem cell lineages. During asymmetric division of a type II neural stem cell (neuroblast) in the Drosophila larval brain, the Brain tumor (Brat) protein segregates unequally into the immature intermediate neural progenitor (INP), where it specifies INP identity by attenuating the function of the self-renewal factor Klumpfuss (Klu), but the mechanisms are not understood. Here, we report that Brat specifies INP identity through its N-terminal B-boxes via a novel mechanism that is independent of asymmetric protein segregation. Brat-mediated specification of INP identity is critically dependent on the function of the Wnt destruction complex, which attenuates the activity of β-catenin/Armadillo (Arm) in immature INPs. Aberrantly increasing Arm activity in immature INPs further exacerbates the defects in the specification of INP identity and enhances the supernumerary neuroblast mutant phenotype in brat mutant brains. By contrast, reducing Arm activity in immature INPs suppresses supernumerary neuroblast formation in brat mutant brains. Finally, reducing Arm activity also strongly suppresses supernumerary neuroblasts induced by overexpression of klu. Thus, the Brat-dependent mechanism extinguishes the function of the self-renewal factor Klu in the presumptive intermediate progenitor cell by attenuating Arm activity, balancing stem cell maintenance and progenitor cell specification.
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