Mitochondrial Signaling

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Presentation transcript:

Mitochondrial Signaling Ronald A Butow, Narayan G Avadhani Molecular Cell Volume 14, Issue 1, Pages 1-15 (April 2004) DOI: 10.1016/S1097-2765(04)00179-0

Figure 1 Retrograde Induction of Metabolic Pathways in Respiratory-Deficient Cells The retrograde pathway enables respiratory-deficient cells to maintain glutamate supplies by providing substrates for α-ketoglutarate synthesis through anaplerotic pathways and increased transport into cells of glutamate and alternative nitrogen sources. Molecular Cell 2004 14, 1-15DOI: (10.1016/S1097-2765(04)00179-0)

Figure 2 Regulation of RTG-Dependent Gene Expression Positive and negative regulators of the RTG pathway and interactions with TOR signaling are shown. TOR is proposed to regulate the SPS amino acid sensor system that acts upstream of Rtg2. Expression of RTG genes also regulates the formation of [URE3] (Sekito et al., 2002), which is an inactive form of a negative regulator of the NCR pathway, Ure2 (Wickner, 1994). Molecular Cell 2004 14, 1-15DOI: (10.1016/S1097-2765(04)00179-0)

Figure 3 Regulation of RTG-Dependent Gene Expression by a Dynamic Interaction between Rtg2p and the Negative Regulator Mks1p Mks1p, when bound to Rtg2p, is inactive; Mks1p bound to the 14-3-3 proteins Bmh1p and Bmh2p is the form that prevents Rtg1p and Rtg3p from translocating from the cytoplasm to the nucleus. Molecular Cell 2004 14, 1-15DOI: (10.1016/S1097-2765(04)00179-0)

Figure 4 Retrograde Signaling in Mammalian Cells Occurs through Increased Cytosolic Ca2+ Disruption of Δψm by various causes affects mitochondrial uptake of Ca2+ and reduced efflux into storage organelles or outside the cells due to reduced availability of ATP. Increased cytosolic Ca2+ in turn activates calcineurin and various Ca2+-dependent kinases. Molecular Cell 2004 14, 1-15DOI: (10.1016/S1097-2765(04)00179-0)

Figure 5 Activation of Cytoplasmic and Nuclear Factors in Different Cell Systems in Response to Mitochondrial Stress Induced by Different Causes Increased cytoplasmic free Ca2+ in different cell systems activates protein phosphatase, calcineurin, and Ca2+-sensitive kinases, PKC, JNK, MAPK, and CamKIV, which in turn activate different nuclear transcription factors. Molecular Cell 2004 14, 1-15DOI: (10.1016/S1097-2765(04)00179-0)

Figure 6 Mechanism of Mitochondrial Stress-Induced Activation of NFκB through Ca2+ Activated calcineurin binds to IkBβ-heteromeric Rel protein complex through the C-terminal PEST domain of IkBβ. Phosphorylation of PEST domain Ser residues by CKII or other kinases is critical for calcineurin binding. Calcineurin-mediated dephosphorylation of IkBβ causes the release of active Rel dimers, which translocate to the nucleus. IkBβ released from the complex is either recycled or degraded probably by ubiquitination. Molecular Cell 2004 14, 1-15DOI: (10.1016/S1097-2765(04)00179-0)