Figure 9.

JNK-dependent puc-lacZ induction by Slpr and Tak1 in adult female fat body. (A) X-gal staining of adult female abdominal fillets showing induction of puc-lacZ as indicated by the blue product upon expression of various transgenes compared to a Gal4-only control (no Tg) in the absence (left column) or presence (right column) of E. coli infection. Cells of the dorsal vessel have endogenous galactosidase activity. (Ai) Quantification of β-gal staining intensity in arbitrary units is shown as a floating bar graph representing minimum to maximum values for 5–22 individuals with a vertical line at the mean. Data from two independent transgenes were combined. Transgene identities are aligned with the corresponding stained images from A. All pairwise comparisons of puc-lacZ induction, with and without E. coli challenge, are not significantly different; however, all the individual means compared to the control (without infection) are significantly different except Tak1^K46R. Analysis by ANOVA with Bonferroni post-test (P < 0.05). (B and Bi) Magnified images of X-gal staining across one abdominal segment in the fat body (fb) and oenocytes (oe) in response to expression of wild-type Slpr (B) or Tak1 (Bi) using the Yp1-Gal4 driver. Tak1 expression results in disorganization and progressive loss of fat body tissue. Bar, 100 μm.