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p53- and ERK7-Dependent Ribosome Surveillance Response Regulates Drosophila Insulin-Like Peptide Secretion

Figure 1

Kinome-wide screen identifies novel regulators of IPCs.

(A) Overview of the kinome-wide RNAi screen in the IPCs. Each point indicates the mean body weight of RNAi expressing flies normalized to weight of flies from the same vial that do not express RNAi in the IPCs (i.e. relative weight). Dotted lines indicate +/−10% of the median body weight. (B) Kinome-wide RNAi screen identifies 12 kinases whose knockdown in the IPCs by two independent RNAi lines leads to significantly reduced body weight. Error bars represent standard deviation (N≥3, ≥10 flies/group). (C) TORC1 is essential for normal IPC function. Knockdown of Raptor, but not Rictor, in IPCs leads to reduction in body weight. Error bars represent standard deviation (N = 4, ≥10 flies/group). (D) Relative mRNA expression of dilp2, dilp3, and dilp5 upon knockdown of the kinase hits. Knockdown of Raptor, instead of TOR, was used to inhibit TORC1 function. Error bars represent standard deviation (N = 3, 10 brains/group). GAPDH was used as an internal reference. *p<0.05, **p<0.01, ***p<0.001 (Student's t-test).

Figure 1

doi: https://doi.org/10.1371/journal.pgen.1004764.g001