Please use this identifier to cite or link to this item: https://doi.org/10.7554/eLife.01906
Title: The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
Authors: Koe, C.T.
Li, S.
Rossi, F.
Wong, J.J.L.
Wang, Y.
Zhang, Z.
Chen, K.
Aw, S.S.
Richardson, H.E.
Robson, P.
Sung, W.-K. 
Yu, F. 
Gonzalez, C.
Wang, H. 
Issue Date: 11-Mar-2014
Citation: Koe, C.T., Li, S., Rossi, F., Wong, J.J.L., Wang, Y., Zhang, Z., Chen, K., Aw, S.S., Richardson, H.E., Robson, P., Sung, W.-K., Yu, F., Gonzalez, C., Wang, H. (2014-03-11). The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages. eLife 2014 (3) : -. ScholarBank@NUS Repository. https://doi.org/10.7554/eLife.01906
Abstract: 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. © Koe et al.
Source Title: eLife
URI: http://scholarbank.nus.edu.sg/handle/10635/110299
ISSN: 2050084X
DOI: 10.7554/eLife.01906
Appears in Collections:Staff Publications

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