Fig. 4

Proposed mechanism explaining how P. rhodozyma cells sense and develop an adaptive response to environmental cues, or to mutations in genes impairing respiration. The mechanism rationalizes the central role that redox imbalances play along with changes in mitochondrial pO₂, to generate a dynamic redox signal that inform the yeast cells about changing environmental conditions and mutations. The dynamic redox signal serves to steadily tune an adaptive response. Copper deficiency, respiratory inhibitors (e.g., antimycin-A), low mitochondrial pO₂ level and mutations impairing respiration, all are events leading to similar sequential outcomes, (i) slow oxygen uptake rate concurrently with slow NADH conversion to NAD⁺, (ii) increasing mitochondrial pO₂ together with more reduced state of cofactors (NADH/NAD⁺ and QH₂/Q couples) of the main electron transport chain, (iii) augmented O^2·−/H₂O₂ formation as a result from the events ii, each one on its own, (iv) antioxidant response induction (e.g., astaxanthin synthesis and, asy and aox expression), and (v). induction of alcoholic fermentation (low oxygen levels triggers anaerobic fermentation, whereas copper deficiency triggers aerobic fermentation). Ethanol consumption at the diauxic shift leads to a NADH surplus as primary outcome of a faster NADH replenishment (red arrow, to emphasize that the primary source of the redox imbalance is not an impaired respiration at first), and secondly, to an impaired oxygen consumption as a result of NAD⁺ deficit (for clarity not shown in the figure). Successively these events lead to similar outcomes as those cited in ii–iv above. Induction of fermentation (v) does not occur in this case, but may be functional when the faster NADH replenishment comes from increasing glucose concentrations [71]