Environmental effects on picloram uptake and ethylene production by broom snakeweed.

Abstract

Broom snakeweed [Gutierrezia sarothrae (Pursh) Britt. &Rusby] is a rangeland weed widely distributed in the western United States. Picloram (4-amino-3,5,6-trichloro-2-pyridinecarboxylic acid) uptake and picloram-induced ethylene production by broom snakeweed grown in the field were determined every 2 to 4 weeks over 36 months. For each collection date, picloram uptake and concentration in the tissue ranged from 1.5 to 46.2% of applied and 0.2 to 4.7 nmol g-1 fresh wt, respectively. Of the measured environmental variables, average precipitation and average minimum temperature 7 days prior to treatment best predicted picloram uptake and concentration in the tissue, suggesting that warmer temperatures and precipitation previous to application contribute to picloram uptake. Average minimum temperature alone also provided a good predictor for picloram concentration in the tissue. For each collection date, picloram-induced ethylene production by total tissue ranged from 50 to 791% of control. Picloram-induced ethylene production by total tissue was best predicted by the precipitation and minimum temperature 7 days prior to treatment and picloram concentration in the tissue. Therefore, the amount of picloram absorbed and the environment prior to application both contribute to the physiological sensitivity of broom snakeweed to picloram. Picloram uptake and picloram-induced ethylene production were greatest in July and August, when plants were in the phenological stages of shoot regreening or flower bud emergence and when temperatures and precipitation were high. Previous field studies have shown broom snakeweed is most responsive to field picloram application in the post-bloom stage from October to December or in April and May with high moisture and soil temperature conditions; therefore, it appears that changes in uptake and physiological sensitivity as measured by picloram-induced ethylene production are not the only factors controlling differential sensitivity to picloram.