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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Biochim Biophys Acta. 2013 Jan 2;1827(5):10.1016/j.bbabio.2012.12.007. doi: 10.1016/j.bbabio.2012.12.007

Figure 4.

Figure 4

Complex II/mKATP interaction in energy sensing: “Classical” respiratory coupling is shown in the center, in which mitochondria transition between quiescent (state 4) and phosphorylating (state 3) conditions depending on availability of ADP. Additional levels of control are shown in outer circuits, including: (i) ATP is a complex II activator, so low ATP leads to preferred electron entry via complex I, which in turn increases the efficiency/stoichiometry of Ox-Phos (H+/e− ratio), increasing ATP synthesis (right side). The reverse is true when ATP is high (left side). (ii) Low ATP dis-inhibits (opens) the mKATP channel, leading to K+ and water entry and swelling of the matrix (right side). This leads to greater contact between the inner and outer membranes (IM/OM), enhancing the creatine kinase shuttle and ATP availability for the cell. When ATP is low, the cycle reverses, as ATP closes the mKATP channel, the matrix shrinks, and IM/OM contact decreases, lowering ATP transport to the cytosol (left side).