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|Title:||The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages||Authors:||Koe, C.T.
|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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