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First published online July 5, 2006
doi: 10.1242/10.1242/jcs.03062

Journal of Cell Science 119, 2855-2862 (2006)
Published by The Company of Biologists 2006
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Nitric oxide and mitochondrial biogenesis

Enzo Nisoli* and Michele O. Carruba

Department of Pharmacology, Chemotherapy and Medical Toxicology, School of Medicine, Milan University, via Vanvitelli, 32, 20129 Milan, and Istituto Auxologico Italiano, via Spagnoletto, 3, 20149 Milan, Italy


Figure 1
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  		Fig. 1. Mitochondrial fusion and fission dissected. (A) Fusion of mitochondria requires the sequential interaction of outer and inner membranes. Fusion of the outer membranes of two adjacent mitochondria requires low GTP levels, whereas the subsequent fusion of the inner membranes requires high GTP levels. Two components of the mitochondrial fusion machinery are known in mammalian cells, the outer membrane proteins mitofusins Mfn1 and Mfn2, which each have a cytosolic GTPase domain and two coiled-coil regions, and the intermembrane space proteins GTPase OPA1. (B) Models and molecules of mitochondrial fission. Fission protein 1 (Fis1) is localized uniformly to the mitochondrial outer membrane, whereas dynamin-related protein (Drp1) is localized to the cytosol and punctate spots on mitochondria. Some of these spots are constriction sites that lead to mitochondrial fission. How Drp1 is recruited to mitochondria is unclear.

 

Figure 2
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  		Fig. 2. Calorie restriction induces cGMP production through an increase in eNOS levels in white adipose tissue and other mouse tissues. Nuclear genes involved in mitochondrial biogenesis, including PGC-1{alpha}, are upregulated as a consequence, leading to increased mitochondrial biogenesis, as well as resistance to stress and diminished fat synthesis, mainly throughout SIRT1 gene expression.

 

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© The Company of Biologists Ltd 2006