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 2. Failure to restrict the competence of progenitors to respond to self-renewal factors allows them to revert to form CSCs.

Figure 2

(A) Lineage diagram depicting tumorigenesis when erm or the SWI/SNF complex is mutated. INPs possess extended competence (salmon box) to respond to normal reactivation (light blue box) of self-renewal factors, causing INPs to revert to form supernumerary neuroblasts. Thus, INPs serve as the cell of origin (brown triangle), and revert to form supernumerary neuroblasts that likely act as the CSCs (purple diamond). In erm or SWI/SNF mutants type II neuroblasts, immature INPs, INPs and supernumerary neuroblasts retain tumorigenic potential (grey box) whereas, GMCs, and Diff. cells do not. (B) Confocal image showing Erm expression pattern (green). The following are indicated: type II neuroblast (white arrow); immature INPs (white arrowhead); and INP (yellow arrow). (C) Schematic showing Erm (green) and the SWI/SNF complex (yellow) remodeling the chromatin to restrict the competence to respond to the self-renewal network: nucleasome (grey oval); DNA (black line).