Greenhouse studies were conducted in 2003 at the Stine–Haskell Research Center to determine whether herbicide inhibitors of six specific sites in the carotenoid biosynthesis pathway would elicit synergistic responses when applied postemergence (POST) in combination with the photosystem II (PSII) inhibitor atrazine. Based on data analysis with the Isobole method, synergistic responses were observed on red morningglory, common cocklebur, and giant foxtail when atrazine was applied in mixtures with the deoxy-D-xylulose-5-phosphate reductoisomerase (DOXP reductoisomerase) inhibitor fosmidomycin, thep-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor mesotrione, and the DuPont proprietary zeta-carotene desaturase (ZDS) inhibitor DFPC. Clomazone (its metabolite ketoclomazone is the actual enzyme inhibitor), an inhibitor of 1-deoxy-D-xylulose-5-phosphate synthatase (DOXP synthase), provided synergistic responses on red morningglory, but antagonistic responses on both common cocklebur and giant foxtail when applied in mixtures with atrazine. Combinations of the lycopene cyclase (LC) inhibitor, CPTA, with atrazine produced synergistic responses on both common cocklebur and giant foxtail but were antagonistic on red morningglory. Norflurazon, a phytoene desaturase (PDS) inhibitor, applied in mixtures with atrazine provided synergistic responses on red morningglory, antagonistic responses on giant foxtail, and independent responses on common cocklebur. Because carotenoids have been determined to play a key role in quenching singlet oxygen species in the chloroplast and also assist in the maintenance of the D1 protein in PSII, this might help explain the synergistic responses with atrazine observed in our studies.

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Studies were conducted to determine how a serine to threonine mutation at position 264 on the Qb binding niche of the D1 protein [urea-resistant/triazine resistant (UR/TR biotype)] in common purslane (Portulaca oleracea) impacted carotenoid and chlorophyll pigment pools and measurements of photochemical and non-photochemical quenching (NPQ) following applications of various inhibitors of carotenoid biosynthesis (CBI) and the Photosystem II (PSII) inhibitor diuron when applied alone, or in mixtures, as compared to wildtype (WT) purslane. Non-photochemical quenching decreased 138 to 531% in comparison to the untreated checks following any herbicide application. Most CBI herbicides and diuron did not change chl a and chl b in the UR/TR biotype, while these same herbicide treatments tended to sharply decrease chlorophyll pigments in the WT population. Zeaxanthin levels were sharply elevated when CBI herbicides were applied alone to both purslane biotypes. β-carotene reduced in both biotypes following herbicide applications in comparison to the untreated check. Neoxanthin, antheraxanthin, and lutein were generally increased or remained similar to the untreated controls in the herbicide treated UR/TR biotype, while levels of these carotenoids tended to decrease in the herbicide treated WT population. Diuron alone increased neoxanthin, antheraxanthin, lutein, and zeaxanthin by 4 to 200% in the UR/TR biotype, but decreased these same carotenoids 25 to 62% in the WT population. The applications of CBI and PSII herbicides demonstrate that redox signaling in response to this mutation in the D1 protein may impact the retention of plant pigment concentrations in the light harvesting complexes of PSII, which would be vital for stress tolerance in this biotype.