Please use this identifier to cite or link to this item: https://doi.org/10.1002/embr.201337966
Title: The SCFSlimb E3 ligase complex regulates asymmetric division to inhibit neuroblast overgrowth
Authors: Wang, H. 
Li, S.
Wang, C.
Sandanaraj, E.
Aw, S.S.Y.
Koe, C.T.
Wong, J.J.L.
Yu, F. 
Ang, B.T. 
Tang, C. 
Keywords: asymmetric division
neuroblasts
polarity
the SCF complex
Issue Date: 2014
Citation: Wang, H., Li, S., Wang, C., Sandanaraj, E., Aw, S.S.Y., Koe, C.T., Wong, J.J.L., Yu, F., Ang, B.T., Tang, C. (2014). The SCFSlimb E3 ligase complex regulates asymmetric division to inhibit neuroblast overgrowth. EMBO Reports 15 (2) : 165-174. ScholarBank@NUS Repository. https://doi.org/10.1002/embr.201337966
Abstract: Drosophila larval brain neuroblasts divide asymmetrically to balance between self-renewal and differentiation. Here, we demonstrate that the SCF Slimb E3 ubiquitin ligase complex, which is composed of Cul1, SkpA, Roc1a and the F-box protein Supernumerary limbs (Slimb), inhibits ectopic neuroblast formation and regulates asymmetric division of neuroblasts. Hyperactivation of Akt leads to similar neuroblast overgrowth and defects in asymmetric division. Slimb associates with Akt in a protein complex, and SCFSlimb acts through SAK and Akt to inhibit neuroblast overgrowth. Moreover, Beta-transducin repeat containing, the human ortholog of Slimb, is frequently deleted in highly aggressive gliomas, suggesting a conserved tumor suppressor-like function. Synopsis This report provides evidence that loss of the SCFSlimb E3 ubiquitin ligase complex as well as hyperactivation of Akt lead to neuroblast overgrowth and defects in asymmetric cell division. Slimb, the F-box protein of the SCF complex, associates with Akt in a protein complex, and SCFSlimb acts through SAK and Akt to inhibit neuroblast overgrowth. The SCFSlimb E3 ubiquitin ligase inhibits neuroblast (NB) overgrowth and regulates asymmetric division of NBs. The NB overgrowth phenotype in the absence of SCFS limb is similar to what is seen in conditions of AKT hyperactivation. The F-box protein Slimb associates with AKT and regulates NB overgrowth via SAK and AKT. This report provides evidence that loss of the SCFSlimb E3 ubiquitin ligase complex as well as hyperactivation of Akt lead to neuroblast overgrowth and defects in asymmetric cell division. Slimb, the F-box protein of the SCF complex, associates with Akt in a protein complex, and SCF Slimb acts through SAK and Akt to inhibit neuroblast overgrowth. © 2014 The Authors.
Source Title: EMBO Reports
URI: http://scholarbank.nus.edu.sg/handle/10635/110320
ISSN: 14693178
DOI: 10.1002/embr.201337966
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