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. Author manuscript; available in PMC: 2019 Jun 24.
Published in final edited form as: Cell Rep. 2019 May 14;27(7):1979–1990.e7. doi: 10.1016/j.celrep.2019.04.084

Figure 4. dPIP4K Alters PIP3 Turnover by Limiting Class I PI3K Activity.

Figure 4

(A) (i) Reactions influencing PIP3 turnover at the plasma membrane. Insulin activates PI3K, and wortmannin irreversibly inhibits PI3K. (ii) Three phases in the live-imaging assay to follow PIP3 dynamics.

(B) Single live-imaging traces of plasma membrane/cytosolic PIP3 probe fluorescence ratio from salivary glands expressing GFP::PH-GRP1.

(C and D) Comparison of average live-imaging traces of PIP3 probe fluorescence ratios in (C) control and dPIP4K29, and (D) control and dPIP4K overexpression salivary glands (N = 7 imaging runs for all genotypes, minimum of about nine cells analyzed from each run). Error bars: SD. Controls were repeated as the two experiments were performed at different times.

(E) Normalized differences in instantaneous rate of change in fluorescence (ratio of test to that in controls); maximal difference is indicated alongside.

(F) PIP3 levels in wild-type and dPIP4K-overexpressing salivary glands. Live salivary gland PIP3 dynamics upon knockdown of dPIP4K.

See also Figure S5.