FIG. 2.

The loss of bel rescues proliferation of de2f1 mutant cells. Wild-type cells are marked by the presence of GFP (green), while mutant tissue lacks GFP. Clones of mutant cells were induced with ey-FLP and are identified by the lack of GFP (green). (A) Clones of bel^7d19 de2f1⁷²⁹ double-mutant cells. (B and B*) The loss-of-function bel^L4740 mutant allele makes no Bel protein (red), as revealed by the absence of staining with anti-Bel antibody in clones of bel^L4740 mutant cells (absence of green). (B*) The same image as in panel B, showing expression of Bel (red) without GFP. (C) The known loss-of-function bel^L4740 mutant allele rescues proliferation of de2f1 mutant cells. Note the appearance of patches of double-mutant, GFP-negative tissue. (D) The eye discs were labeled with BrdU (red) to visualize S phases. The MF is marked by the arrowhead. Wild-type cells asynchronously cycle anterior to the MF, are arrested in G₁ within the MF, and synchronously enter S phase in the SMW posterior to the MF. The loss of bel partially rescues the SMW in de2f1 mutant cells, as evident by the appearance of bel de2f1 double-mutant BrdU-positive cells in the SMW. (E) Distribution of Bel protein in a wild-type eye disc. Bel is shown in red, and DAPI staining is shown in blue. Bel exhibits a predominantly cytoplasmic distribution.