The American chestnut (Castanea dentata) was an ecologically, economically, and culturally important tree within its natural range in the Eastern United States and Canada. A devastating fungal blight, caused by Cryphonectria parasitica, was introduced from Asia in the late 1800’s that lead to the mortality of over three billion American chestnut trees. Researchers at the State University of New York College of Environmental Science and Forestry (SUNY-ESF) developed a blight-tolerant American chestnut tree by inserting a wheat gene, coding for the enzyme oxalate oxidase (OxO), into its genome. This enzyme detoxifies oxalic acid, preventing the fungus from producing lethal cankers. A decade of ecological research has investigated potential non-target effects of this transgene, demonstrating a lack of effects on mycorrhizal colonization, insect herbivory, and pollen use by bees. Here we ask: do transgenic American chestnuts differ in their physiological ecology relative to non-transgenic American chestnuts? We report on two years of physiological assessment of field-grown transgenic and non-transgenic American chestnut trees, with measurements of photosynthetic CO2 and light response curves, mitochondrial respiration in the light and the dark (Rlight and Rdark), and foliar traits (specific leaf area, SLA; foliar N content).
Results/Conclusions
There was no evidence that the photosynthetic physiology of American chestnut trees differed between transgenic and non-transgenic varieties. Photosynthetic capacity was equivalent, with values reflective of fast growing trees of intermediate shade tolerance (Vc,max averaged 46.5, Jmax averaged 80.3, Asat averaged 15, and the light-compensation point averaged 25, all units are µmol m-2 s-1). There was, however, an increased rate of Rdark in transgenic trees compared to non-transgenic trees (+20%; P < 0.05). This was particularly apparent in the temperature response of Rdark, in which there was a consistent stimulation of Rdark in transgenic trees across a range of temperatures from 10-25 °C. Rlight, however, was equivalent across the groups with an average of -0.8 µmol m-2 s-1. The stimulation of Rdark in the transgenic trees may not be large enough to be biologically significant, as the transgenic and non-transgenic trees did not differ in rates of height and diameter growth (~40 cm height growth yr-1 and 6 mm diameter growth yr-1; P > 0.1). Thus, we conclude that the transgene may invoke a minor metabolic cost that stimulates Rdark, but that this effect is unlikely to be large enough to fundamentally change the physiological ecology of this keystone species.