Paclobutrazol affects the resistance of black spruce to high light and thermal stress

Detached needles from 20-week-old black spruce (Picea mariana (Mill.) B.S.P.) seedlings root-drenched with 60 mg of paclobutrazol were exposed to two temperatures (22 and 50 degrees C) and two light treatments (100 and 1900 &mgr;mol m(-2) s(-1) PAR) in a factorial combination for 4 h in vitro. Mean dry weights of individual needles from paclobutrazol-treated plants were approximately 1.9 times heavier than that of needles from untreated controls at 22 degrees C, but no differences were observed following incubation at 50 degrees C. Numbers of cells per needle remained constant in all treatments. Chlorophyll and carotenoid contents per needle were higher in seedlings treated with paclobutrazol than in untreated control seedlings, and the differences were most pronounced in the high temperature plus high light treatment. In low light at 50 degrees C, quantum efficiency of photosystem II was 45% higher in needles of paclobutrazol-treated seedlings than in needles of untreated control seedlings, but quantum efficiency of needles from treated seedlings declined when needles were exposed to high light at either temperature. Peroxidase and superoxide dismutase activities were up-regulated by paclobutrazol, whereas catalase activities were depressed and no significant differences were observed between treated and control needles at 50 degrees C in either light treatment. Paclobutrazol treatment did not moderate the depressive effects of high temperature on total soluble protein or on the activity of ribulose-1,5-bisphosphate carboxylase. In contrast, high activities of phosphoenolpyruvate carboxylase were maintained in paclobutrazol-treated needles under all stress conditions, whereas large losses in activity were recorded in untreated needles at 50 degrees C. Collectively, these observations suggest that paclobutrazol treatment may convey resistance to excessive light and high temperatures by increasing the potential of conifers to limit damage caused by oxidative stress.