97th ESA Annual Meeting (August 5 -- 10, 2012)

COS 86-5 - Methanol production and emission by plants in response to damage and wounding

Wednesday, August 8, 2012: 9:20 AM
E144, Oregon Convention Center
Patricia A. Oikawa1, Lei Li2, Michael Timko2, John Mak3 and Manuel Lerdau4, (1)1Department of Botany and Plant Sciences, University of California, Riverside, Riverside, CA, (2)Departments of Environmental Sciences and Biology, University of Virginia, Charlottesville, VA, (3)Marine Sciences, State University of New York, Stony Brook, NY, (4)Departments of Environmental Sciences and of Biology, University of Virginia, Charlottesville, VA
Background/Question/Methods

Plants produce a wide variety of low molecular weight compounds that have high enough vapor pressures to volatilize at physiologically realistic temperatures and enter the atmosphere.  Once in the atmosphere, these compounds play crucial roles in the chemical and radiative properties of the troposphere, including the redox balance of the lower atmosphere and the formation of aerosols.  These volatile compounds result from a wide variety of biosynthetic routes and serve a broad range of functions within plants.  Most attention to date has concentrated on those compounds involved with plant defense against herbivores and those that appear to protect against thermal or oxidative damage.  There appear, however, to be other compounds that are produced simply as by-products of metabolism.  We investigate the production and emission of one such compound, methanol (CH3OH, or MeOH), whose production is tied to cell wall metabolism, to try and understand its production in both genetic and ecological contexts so that better predictive models of emission can be constructed.  We bring together molecular, enzymatic, and physiological methods to study production and emission in both wild-type and genetically transformed tomato (Lycopersicon esculentum Mill.) plants.  By examining the responses of gene expression, enzyme activity, and flux rate to wounding across time scales, we are able to gain a better understanding of MeOH production and emission controls.

Results/Conclusions

Elevated MeOH emissions observed 10 min and 1 hr post wounding were not associated with up-regulated gene expression or enzyme activity and were therefore attributed to decreased diffusive barriers resulting from damaged leaf tissue.  Surprisingly, we found local and systemic down-regulation of MeOH candidate genes over the first 24 hours after wounding, suggesting that repair processes that involve MeOH synthesis have not been initiated during this time.  Using wild type and mutant tomato (Lycopersicon esculentum Mill.) with a deficient jasmonic acid (JA) signaling system, long-term and systemic MeOH candidate gene transcription responses to wounding were found to be JA-independent.  This result argues for the independence of cell wall processes from the first stages of plant response to damage and is congruent with the idea that there may be strong genetic, as well as temporal, separation between defensive and regenerative processes in plants.  Further increases in our understanding of MeOH production and emission controls require that we examine the complete array of genetic and biochemical processes that may underlie its biosynthesis.