Abstract

Interest in modeling isoprene emission from vegetation has led to the development and widespread use of an emission algorithm (referred to here as the G93 algorithm) that estimates instantaneous leaf isoprene emission as a function of basal isoprene emission rate with corrections for the effects of light and temperature. Here we address the question: Does the G93 algorithm reflect the biochemical and physiological processes responsible for leaf isoprene emission? In particular, the activity of the enzyme isoprene synthase, thought to be responsible for leaf isoprene emission, is examined. Recent findings show that isoprene synthase activity in willow leaves is located in chloroplasts, where both soluble and thylakoid‐bound forms of the enzyme occur. Short‐term changes in the activity of the isoprene synthases in response to temperature are consistent with the temperature correction term of the G93 algorithm. The light dependence term of the algorithm, which predicts light saturation of leaf isoprene emission, is consistent with the plastidic location of the isoprene synthases and light‐driven processes responsible for activation of enzymes. However, the complete mechanism for the light activation of isoprene synthase(s) has not been determined. Long‐term changes in the amount of active isoprene synthase(s) correlate with the variations in basal isoprene emission rate seen as leaves mature and adapt to differences in leaf growth environment. Despite these correlations, recent reports that the G93 algorithm can be used to model light‐dependent formic acid, 2‐methyl‐3‐buten‐2‐ol and monoterpene emissions raise questions about the algorithm's specificity and underlying assumptions.

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