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Graphical model of inferred consequences of UNC‐105 activation upon muscle mitochondria and cytosol. The UNC‐105 ion channel, when not gated by LET‐2, allows excess ion influx into muscle. In response to sustained ion influx, mitochondria are dysfunctional, and cytochrome C and CED‐4 translocate from the mitochondria. Translocated CED‐4 interacts with CED‐3 to cause CED‐3 activation. Activated CED‐3 causes cytosolic protein degradation.
