Figure 8.

Rescue of the β-spectrin overexpression phenotype in the fat body. Males carrying X-linked UAS-β-Spec⁶² and heterozygous for autosomal UAS‐α‐Spec³⁷ (UAS-β-Spec⁶²/Y; UAS‐α-Spec³⁷/+) were crossed to females homozygous for autosomal Cg-Gal4 (+/+; Cg‐Gal4/Cg-Gal4) at 25°. (A) In control crosses, expression of UAS‐β-Spec⁶² alone at 25° resulted in 100% larval lethality at second instar and expression of UAS‐α-Spec³⁷ alone had no effect on larva viability. However, in rescue crosses with α- and β-spectrin transgenes together, female progeny could be recovered as third instar larvae and they were 100% viable to adulthood. (B and C) These third instar female progeny exhibited dramatically elevated β-spectrin staining in the fat body (C) compared to their male siblings that did not express the β-spectrin transgene (B, same microscope setting as in C). Insets show lipid droplets in wild-type fat body by DIC (B) and their return after rescue of β overexpression by α-spectrin (C). (D–F) Oil Red O staining of dissected second instar larvae. The midgut lipid droplet accumulation observed with β-spectrin overexpression alone (E) was not seen in larvae expressing both β- and α-spectrin (F), although lipid staining was apparent in the fat body (arrowhead). A male sibling from the rescue cross not expressing excess β-spectrin is shown as a negative control (D). Bar, 50 µm.