AI Article Synopsis
- Drosophila larval brain neuroblasts undergo asymmetric division to maintain a balance between self-renewal and differentiation.
- The SCF(Slimb) E3 ubiquitin ligase complex is crucial in preventing excessive neuroblast formation and ensuring proper asymmetric division.
- Hyperactivation of the Akt pathway mimics neuroblast overgrowth, and Slimb's interaction with Akt suggests it may serve a tumor suppressor role, supported by its deletion in aggressive gliomas.
Article 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 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3989862 | PMC |
| http://dx.doi.org/10.1002/embr.201337966 | DOI Listing |
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