Figure 6.
Notch activity is up-regulated in aurA mutants and Notch is necessary and sufficient for NB self-renewal. (A–B′) Overexpression of activated Notch (the intracellular domain of Notch, Nact) induced NB overgrowth and tumor formation. (A′,B′) Mitotic clones were marked by β-galactosidase (β-Gal). In Nact clones, most cells express Mira (B), whereas only one cell (NB) expresses Mira in control clone (A). (C) Quantification of the number of cells per clone in control and activated Notch clones. (D,D″) Spdo localization in wild-type (D), numb15 (D′), and aurA8839 (D″) mutant larval NBs. (D) In wild-type NBs, Spdo is mostly observed as weak punctate structures on the cortex as well as throughout the cytoplasm. In numb15 (D′) and aurA8839 (D″) mutants, Spdo is almost exclusively localized at the cortex. (E,E′) Notch levels indicated by an antibody against its intracellular domain are up-regulated in aurA mutant brains (E′) compared with wild type (E). (F,F′) Notch is a critical proliferation factor for larval NBs. Notchts-1 third instar larval brains (68 h ALH, 29°C from larval hatching) contain fewer NBs, marked by Dpn in green (F′) compared with wild type (F). Note that wild-type larval NBs exhibit either nuclear (arrow) or cytosolic (arrowhead) Dpn signals, whereas most of the Notchts-1 larval NBs exhibit nuclear (arrow) but not cytosolic Dpn. (G) Quantification of NB numbers per brain lobe for wild type and Notchts-1. Genotypes are hs-FLP; actin-FRT-y+-FRT-Gal4, UAS-nlsLacZ(A,A′), and hs-FLP; actin-FRT-y+-FRT-Gal4, UAS-nlsLacZ/UAS-Nact (B,B′).