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. 2017 Jan 30;7(3):1049–1060. doi: 10.1534/g3.117.039065

Figure 2.

Figure 2

Ectopically-expressed Yki differentially upregulates CycE in the wing disc. (A–B’’’) The CycE reporter CycE-lacZ experiments: (A) CycE-lacZ was examined upon ectopic activation of Yki (A’). CycE-lacZ shows a higher signal intensity in the pouch region (A and A’’’). As a control, in the wild-type wing disc, the CycE reporter shows the endogenous pattern of CycE (B and B’’’). (C–D’’’) The Diap1 reporter Diap1-GFP experiments: (C) was examined upon ectopic activation of Yki (C’). Diap1-GFP shows signals with higher intensity in the ykiM123 expressing cells than the wild-type cells and this upregulation is in both pouch and hinge (C and C’’’). As a control, in the wild-type wing disc, the Diap1 reporter shows the endogenous pattern of Diap1 (D and D’’’). (E–F’’) the expanded reporter ex-lacZ experiments: (E) ex-lacZ was examined upon ectopic activation of Yki (E’). ex-lacZ shows signals with higher intensity in the ykiM123 expressing cells than the wild-type cells and this upregulation is in both pouch and hinge (E and E’’’). As a control, in the wild-type wing disc, the expanded reporter shows the endogenous pattern of ex (F and F’’’). The scale bar is 50 cm. (G–I’) Quantifications of the signal intensity of CycE-lacZ, Diap1-GFP, and ex-lacZ demonstrating that Yki activation fails to significantly upregulate CycE in the hinge (n = 10, error bars are SE values). CycE, Cyclin E; GFP, green fluorescent protein; N.S., no significant difference; RFP; red fluorescent protein; Yki, Yorkie.