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. Author manuscript; available in PMC: 2023 Mar 15.
Published in final edited form as: Exp Cell Res. 2022 Jan 29;412(2):113043. doi: 10.1016/j.yexcr.2022.113043

Figure 9. Inhibition of PI3K signaling induces premature loss of mitochondria.

Figure 9.

E12 lenses were treated for 24 hrs in organ culture with the pan-PI3K inhibitor LY294002, the pan-PI3K inhibitor CH5132799, or their vehicle DMSO. (A) Lens fiber cell fractions isolated from control and inhibitor treated lenses were immunoblotted for TOM20 and (B) the immunoblot results quantified from 3 independent studies. (C) Confocal imaging of cryosections of E12 lenses following exposure for 24 hrs to the the pan-PI3K inhibitor CH5132799 or its vehicle DMSO immunolabeled for TOM20. (D) Confocal imaging of cryosections of E12 lenses following exposure for 24 hrs to the the pan-PI3K inhibitor LY294002 or its vehicle DMSO immunolabeled for TOM20. Line scan analyses were performed across the entire width of the lenses and the fluorescence intensity quantified from 3 independent experiments in the cortical fiber region FP (Ci,Di) denoted as A, and the central fiber region FC (Cii, Dii) denoted by B. The data with two independent PI3K inhibitors shows that blocking PI3K signaling induces premature loss of the mitochondria to form the OFZ. Scale bar, 100 μm. Error bars represent S.E., *P ≤ 0.05, **P ≤ 0.01, and ***P ≤ .001, t test.