The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages

The control of self-renewal and differentiation of neural stem and progenitor cells is a crucial issue in stem cell and cancer biology. Drosophila type II neuroblast lineages are prone to developing impaired neuroblast homeostasis if the limited self-renewing potential of intermediate neural progeni...

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Main Authors: Chwee Tat Koe, Song Li, Fabrizio Rossi, Jack Jing Lin Wong, Yan Wang, Zhizhuo Zhang, Keng Chen, Sherry Shiying Aw, Helena E Richardson, Paul Robson, Wing-Kin Sung, Fengwei Yu, Cayetano Gonzalez, Hongyan Wang
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2014-03-01
Series:eLife
Subjects:
Online Access:https://elifesciences.org/articles/01906
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author Chwee Tat Koe
Song Li
Fabrizio Rossi
Jack Jing Lin Wong
Yan Wang
Zhizhuo Zhang
Keng Chen
Sherry Shiying Aw
Helena E Richardson
Paul Robson
Wing-Kin Sung
Fengwei Yu
Cayetano Gonzalez
Hongyan Wang
author_facet Chwee Tat Koe
Song Li
Fabrizio Rossi
Jack Jing Lin Wong
Yan Wang
Zhizhuo Zhang
Keng Chen
Sherry Shiying Aw
Helena E Richardson
Paul Robson
Wing-Kin Sung
Fengwei Yu
Cayetano Gonzalez
Hongyan Wang
author_sort Chwee Tat Koe
collection DOAJ
description The control of self-renewal and differentiation of neural stem and progenitor cells is a crucial issue in stem cell and cancer biology. Drosophila type II neuroblast lineages are prone to developing impaired neuroblast homeostasis if the limited self-renewing potential of intermediate neural progenitors (INPs) is unrestrained. Here, we demonstrate that Drosophila SWI/SNF chromatin remodeling Brahma (Brm) complex functions cooperatively with another chromatin remodeling factor, Histone deacetylase 3 (HDAC3) to suppress the formation of ectopic type II neuroblasts. We show that multiple components of the Brm complex and HDAC3 physically associate with Earmuff (Erm), a type II-specific transcription factor that prevents dedifferentiation of INPs into neuroblasts. Consistently, the predicted Erm-binding motif is present in most of known binding loci of Brm. Furthermore, brm and hdac3 genetically interact with erm to prevent type II neuroblast overgrowth. Thus, the Brm-HDAC3-Erm repressor complex suppresses dedifferentiation of INPs back into type II neuroblasts.
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spelling doaj.art-0793e30af78c4f4c8651717beb850fa32022-12-22T04:32:16ZengeLife Sciences Publications LtdeLife2050-084X2014-03-01310.7554/eLife.01906The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineagesChwee Tat Koe0Song Li1Fabrizio Rossi2Jack Jing Lin Wong3Yan Wang4Zhizhuo Zhang5Keng Chen6Sherry Shiying Aw7Helena E Richardson8Paul Robson9Wing-Kin Sung10Fengwei Yu11Cayetano Gonzalez12Hongyan Wang13NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore; Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, SingaporeNUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore; Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, SingaporeCell Division Group, Institute for Research in Biomedicine, Barcelona, SpainNeuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, Singapore; Temasek Life Sciences Laboratory, Singapore, SingaporeNeuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, Singapore; Temasek Life Sciences Laboratory, Singapore, SingaporeDepartment of Computer Science, National University of Singapore, Singapore, SingaporeNUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore; Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, SingaporeNUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, SingaporePeter MacCallum Cancer Centre, East Melbourne, Australia; Biochemistry and Molecular Biology Department, University of Melbourne, Parkville, Australia; Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Australia; Anatomy and Neuroscience Department, University of Melbourne, Parkville, AustraliaGenome Institute of Singapore, Singapore, Singapore; Department of Biological Sciences, National University of Singapore, Singapore, SingaporeGenome Institute of Singapore, Singapore, Singapore; Department of Computer Science, National University of Singapore, Singapore, SingaporeNUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore; Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, Singapore; Temasek Life Sciences Laboratory, Singapore, Singapore; Department of Biological Sciences, National University of Singapore, Singapore, SingaporeCell Division Group, Institute for Research in Biomedicine, Barcelona, Spain; Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, SpainNUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore; Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School Singapore, Singapore, Singapore; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, SingaporeThe control of self-renewal and differentiation of neural stem and progenitor cells is a crucial issue in stem cell and cancer biology. Drosophila type II neuroblast lineages are prone to developing impaired neuroblast homeostasis if the limited self-renewing potential of intermediate neural progenitors (INPs) is unrestrained. Here, we demonstrate that Drosophila SWI/SNF chromatin remodeling Brahma (Brm) complex functions cooperatively with another chromatin remodeling factor, Histone deacetylase 3 (HDAC3) to suppress the formation of ectopic type II neuroblasts. We show that multiple components of the Brm complex and HDAC3 physically associate with Earmuff (Erm), a type II-specific transcription factor that prevents dedifferentiation of INPs into neuroblasts. Consistently, the predicted Erm-binding motif is present in most of known binding loci of Brm. Furthermore, brm and hdac3 genetically interact with erm to prevent type II neuroblast overgrowth. Thus, the Brm-HDAC3-Erm repressor complex suppresses dedifferentiation of INPs back into type II neuroblasts.https://elifesciences.org/articles/01906neuroblastself-renewaldifferentiationdedifferentiationintermediate neural progenitorDrosophila
spellingShingle Chwee Tat Koe
Song Li
Fabrizio Rossi
Jack Jing Lin Wong
Yan Wang
Zhizhuo Zhang
Keng Chen
Sherry Shiying Aw
Helena E Richardson
Paul Robson
Wing-Kin Sung
Fengwei Yu
Cayetano Gonzalez
Hongyan Wang
The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
eLife
neuroblast
self-renewal
differentiation
dedifferentiation
intermediate neural progenitor
Drosophila
title The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
title_full The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
title_fullStr The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
title_full_unstemmed The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
title_short The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
title_sort brm hdac3 erm repressor complex suppresses dedifferentiation in drosophila type ii neuroblast lineages
topic neuroblast
self-renewal
differentiation
dedifferentiation
intermediate neural progenitor
Drosophila
url https://elifesciences.org/articles/01906
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