Contributors: Linköping University (LIU); Cellules Souches et Développement / Stem Cells and Development; Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS); This work was supported by the Knut and Alice Wallenberg Foundation, Research Grant: (KAW2012.0101, www.wallenberg.com/kaw/), Swedish Research Council, Research Grant: (VR-NT) (621-2010-5214, www.vr.se), and by the Swedish Cancer Foundation, Research Grant: (120531, www.cancerfonden.se).; We are grateful to S. Henikoff, F. Matsuzaki, S. Bray, R. Holmgren, R.S. Howley, J.B. Skeath, J. Posakony, the Developmental Studies Hybridoma Bank at the University of Iowa, The Stowers Institute, and the Bloomington Stock Center for sharing antibodies, fly lines and DNAs. We thank Vanessa Roca and Lydie Couturier for injection and generation of the E(spl)-HLH-mγnull line. A. Angel, H. Ekman, C. Jonsson and A. Starkenberg provided excellent technical assistance
نبذة مختصرة : International audience ; The Notch pathway controls proliferation during development and in adulthood, and is frequently affected in many disorders. However, the genetic sensitivity and multi-layered tran-scriptional properties of the Notch pathway has made its molecular decoding challenging. Here, we address the complexity of Notch signaling with respect to proliferation, using the developing Drosophila CNS as model. We find that a Notch/Su(H)/E(spl)-HLH cascade specifically controls daughter, but not progenitor proliferation. Additionally, we find that different E(spl)-HLH genes are required in different neuroblast lineages. The Notch/Su(H)/E(spl)-HLH cascade alters daughter proliferation by regulating four key cell cycle factors: Cyclin E, String/Cdc25, E2f and Dacapo (mammalian p21 CIP1
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