Responses of leaf respiration to heatwaves

Mitochondrial respiration (R) is central to plant physiology and responds dynamically to daily short-term temperature changes. In the longer-term, changes in energy demand and membrane fluidity can decrease leaf R at a common temperature and increase the temperature at which leaf R peaks (T-max). However, leaf R functionality is more susceptible to short-term heatwaves. Catalysis increases with rising leaf temperature, driving faster metabolism and leaf R demand, despite declines in photosynthesis restricting assimilate supply and growth. Proteins denature as temperatures increase further, adding to maintenance costs. Excessive heat also inactivates respiratory enzymes, with a concomitant limitation on the capacity of the R system. These competing push-and-pull factors are responsible for the diminishing acceleration in leaf R rate as temperature rises. Under extreme heat, membranes become overly fluid, and enzymes such as the cytochrome c oxidase are impaired. Such changes can lead to over-reduction of the energy system culminating in reactive oxygen species production. This ultimately leads to the total breakdown of leaf R, setting the limit of leaf survival. Understanding the heat stress responses of leaf R is imperative, given the continued rise in frequency and intensity of heatwaves and the importance of R for plant fitness and survival.

Automated summary

Mitochondrial respiration is central to plant physiology and responds dynamically to daily temperature changes, but is more susceptible to short-term heatwaves. As leaf temperature rises, catalysis increases driving faster metabolism, despite declines in photosynthesis, leading to protein denaturation and inactivation of respiratory enzymes. Under extreme heat, membranes become overly fluid and enzymes are impaired, ultimately leading to the breakdown of leaf respiration and limiting leaf survival.