Skip to main content
. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Semin Cell Dev Biol. 2014 Mar 11;0:63–69. doi: 10.1016/j.semcdb.2014.03.006

Figure 1. Aberrant expression of self-renewal factors causes uncommitted progenitors to revert to form CSCs.

Figure 1

A) Lineage diagram depicting tumorigenesis resulting from overexpression of self-renewal factors or brat or numb mutation. Type II neuroblasts express a self-renewal network (light blue) that includes Notch (purple), E(spl)mγ(purple), Dpn (blue), and Klu (magenta). Ase− immature INPs remain competent (light purple box) to respond to aberrant expression (salmon box) of the self-renewal factors and can revert to form supernumerary neuroblasts. In these tumor types, Ase− immature INPs act as the cell of origin (brown triangle) and supernumerary neuroblasts are likely the CSCs (purple diamond); these cell types retain tumorigenic potential (grey box). In contrast, INPs do not retain tumorigenic potential in these tumor types, and only divide 5-6 times to generate exclusively GMCs and differentiated cells that express nuclear Pros (green). (B) Brat and Numb repress expression of self-renewal factors in Ase− immature INPs. (Left) Schematic depicting the mitotic division of a type II neuroblast showing: Brat (red) and Numb (blue) are basally segregated into the Ase− immature INP; DNA is shown in yellow; spindle in grey; and centrosomes in black. (Right) Once in the Ase− immature INPs, Brat and Numb act in parallel to inhibit aberrant expression of distinct components of the self-renewal network.