Figure 5.

Scheme of the proposed functional link between the respiratory chain capacities (KCN-sensitive and AOX-dependent) and the skoto-morphogenic programme. In mitochondria, the KCN-sensitive transport of electrons (ETC) from NADH is used for O₂ reduction and ATP production. Only a limited fraction of electrons is diverted to the AOX enzyme for reduction of O₂ without concomitant ATP production. In etiolated rpoTmp, rug3, atphb3 or KCN-treated WT plants, the KCN-sensitive electron flux is strongly decreased, inducing a strong dysfunctional stress (indicated in red). This stress activates the canonical (ANAC017-dependent) mitochondrial retrograde pathway which activates AOX1a expression. It may be supported by yet unknown factors (represented by a yellow oval with question mark). Additional AOX regulation by dysfunctional stress at the level of protein accumulation and modification might be possible (thick black arrow). As ultimate effect the capacity of the AOX-dependent chain is upregulated and more electrons can be diverted by this pathway, releasing the stress (indicated in green). The dysfunctional stress in combination with the highly increased AOX capacity, however, sends a signal via an unknown transmitter (represented by a grey circle with question mark) that triggers the formation of the triple-like response (or parts of it). (Online version in colour.)