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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Autophagy capacity and sub-mitochondrial heterogeneity shape Bnip3-induced mitophagy regulation of apoptosis

Fig. 1

Single mitochondrion dynamics. a Illustration of Bnip3 dual-functionality due to LIR and BH3 domains. ROS and Bcl2/xL (gray boxes) are points of crosstalk between two distinct branches: LIR-induced mitochondrial autophagy (mitophagy) pathway (blue) and apoptosis signaling by activator BH3 proteins (e.g. tBid), which induces Bax-mediated MOMP and cytochrome c release to induce caspase cascade (red). b Level values of the ODE species represent the mitophagy (blue) versus apoptosis (red) activity capacity for a mitochondrion. The shaded areas indicate range of activity as a function of increasing tBid activation (direction of arrows) and 20 % Bnip3 pre-activation. The overlap shows competition between both pathways via Bnip3. c Illustration of Bnip3 mutants with constitutively-active (2SE) and constitutively-inactive (2SA) LIR domain. d Scenarios of increasingly delayed timing of tBid activation (t = 0, 10, 50) for all mutants of Bnip3 with increasing tBid (direction of arrow) activation. e ROS production as a function of different tBid and autophagic vesicles (AV) level combinations for all three Bnip3 mutants

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