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. 2008 Apr;178(4):1947–1971. doi: 10.1534/genetics.108.086983

Figure 6.—

Figure 6.—

Clonal analysis of wts, scrib, roe, ft, and mer; ex. Egg chambers are stained with phalloidin to reveal actin in cellular cortexes (red). (A) Tumor cells accumulate in stratified layers at the anterior and posterior poles of dlgm35/dlgip20 egg chambers, but they do not invade. The tumor cells delaminate toward the germ line and have a rounded, mesenchymal-like morphology. (B–J) Clonal analysis of roe, wts, scrib, ft, and mer; ex. Cells without lacZ or GFP (green) are homozygous mutant for the indicated mutations. (B) roe2 causes small, noninvasive tumors that delaminate toward the germ line (arrow). Most tumors accumulate around the oocyte, but occasionally at the anterior of the egg chamber as well. More typically, anterior roe2 cells remain in the epithelium but have a rounded morphology (arrowheads), like tumor cells that have completely delaminated. (C and D) wtsX1 and scrib673 tumors are similar to dlgm35/dlgip20 tumors. (E–H) Analysis of BLJ proteins α-Spectrin and Dlg in wts and scrib follicle cells. α-Spectrin and Dlg are localized to the BLJ in the native epithelium (arrows). α-Spectrin and Dlg accumulate around the circumference of wts and scrib tumor cells (arrowheads). This lateralized phenotype is indicative of EMT (see text). (I and J) Clones of ft or mer; ex double mutant cells do not develop tumors.