Figure 2. Lpr2 is required for the uptake of neutral lipids during Drosophila vitellogenesis.

(A–B) lpr1 (A) and lpr2 (B) expression in wild-type ovarioles detected by in situ hybridization. Transcripts of both genes were first visible in the nurse cells (n) of stage 8 egg chambers (asterisk) and their levels increased thereafter. lrp1 transcripts were also detected in the follicle cells of mature egg chambers (A, arrow in inset). (C–E) Immunostaining showing Lpr2 protein localization during oogenesis. Lpr2 is first detected at low levels in stage 8 egg chambers, coinciding with the start of vitellogenesis (asterisks in C). (D) Magnification of a stage 10 egg chamber showing expression at the nurse cells (n) and oocyte (o) membranes. Maximal expression was detected at stage 11 egg chambers (E and E', two focal planes). (F–M) Nile red staining of egg chambers (F–H and J–M) and one blastoderm stage embryos (I) to reveal lipid droplets (yellow, nile red dye fluorescence was captured in the green and red channels). (F–I) Wild-type (wt) genotype. Neutral lipids start to accumulate at vitellogenic stages and reach a maximum in blastoderm embryos. Note that near the end of vitellogenesis, nurse cells degenerate and dump their content into the oocyte. (F) stage 9 (asterisk), (G) stage 10 and (H) stage 11 egg chambers. (J–M) stage 10 egg chambers of the indicated genotypes. Accumulation of neutral lipids is reduced in Df(3R)lpr2 (J), Df(3R)lpr1/2 (K, egg chamber outlined) and Df(3R)lpr1/2 germ-line clones (M) and is normal in Df(3R)lpr1 egg chambers (L). The Df(3R)lpr1/2 egg chamber shown in (K) was dissected from young females in which a few egg chambers in each ovary escaped degeneration at mid oogenesis. (N, O) Egg chambers of wild-type (N) and Df(3R)lpr1/2 (O) ovaries stained with DAPI to reveal the nuclei. Several stage 10 egg chambers display nuclear fragmentation in Df(3R)lpr1/2 females (arrows in O). Scale bars: 100 µm. (F–M) shown at the same magnification.