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The SCF Slimb E3 ligase complex regulates asymmetric division to inhibit neuroblast overgrowth
Author(s) -
Li Song,
Wang Cheng,
Sandanaraj Edwin,
Aw Sherry S Y,
Koe Chwee T,
Wong Jack J L,
Yu Fengwei,
Ang Beng T,
Tang Carol,
Wang Hongyan
Publication year - 2014
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1002/embr.201337966
Subject(s) - ubiquitin ligase , microbiology and biotechnology , cell division , division (mathematics) , dna ligase , chemistry , neuroblast , biology , genetics , dna , cell , ubiquitin , gene , arithmetic , mathematics , neurogenesis
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 C ul1, S kpA, R oc1a 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 SCF S limb 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.