The six primary carotenoids found in most plant species include zeaxanthin, antheraxanthin, violaxanthin, lutein, β-carotene, and neoxanthin (Sandmann, 2001). Carotenoids are pigments integrated into light-harvesting complexes of chloroplasts that function as photoprotectants; carotenoids quench free radicals, perform non-photochemical quenching, and dissipate excess heat and light energy (Croce et al., 1999; Demmig-Adams et al., 1996; Frank and Cogdell, 1996). Carotenoids can also function as light-harvesting pigments by channeling photons unabsorbed by the chlorophyll molecule to the reaction center for photosynthesis (Niyogi, 1999; Polle et al., 2001)
Carotenoid synthesis begins with dimerization of the C20 compound geranyl-geranyl pyrophosphate to produce phytoene, the first C40 carotenoid (Buchanan et al., 2000). Phytoene is metabolized to lycopene through a series of desaturation reactions (Buchanan et al., 2000). Branching of the pathway occurs when lycopene is cyclized into α-carotene or β-carotene, and α-carotene forms lutein and lutein-5,6-epoxide (epoxylutein), whereas β-carotene forms neoxanthin and the xanthophyll cycle pigments (zeaxanthin, antheraxanthin, and violaxanthin) (Buchanan et al., 2000; Demmig-Adams et al., 1996).
Mesotrione, topramezone, and tembotrione are herbicides that affect carotenoid biosynthesis by inhibiting HPPD (EC 188.8.131.52), a precursor to plastoquinone and tocopherols (Bollman et al., 2008; Grossman and Ehrhardt, 2007; Mitchell et al., 2001; Pallett et al., 1998; Secor, 1994). Inhibition of HPPD prevents the formation of plastoquinone, a cofactor required for phytoene desaturase to convert phytoene to phytofluene to ζ-carotene and successive carotenoids (Buchanan et al., 2000). Tissue bleaching (i.e., whitening) that occurs after mesotrione, tembotrione, and topramezone application is attributed to a decrease in carotenoid production from reduced phytoene desaturase activity. The lack of tocopherols also contributes to plant death through a decrease in buffering capacity to reactive oxygen species (Matringe et al., 2005).
Topramezone and tembotrione are currently registered for use in corn (Zea mays L.) (Anonymous, 2006, 2009a; Bollman et al., 2008) and are being evaluated for weed control efficacy in turfgrass and ornamentals (Armel et al., 2009; Brosnan et al., 2010). Mesotrione is currently registered for weed control in turf (Anonymous, 2009b) and has been shown to injure common bermudagrass [Cynodon dactylon (L.) Pers.]. McCurdy et al. (2008) and Willis et al. (2007) reported bermudagrass injury with mesotrione ranging from 9% to 44%; however, this injury did not result in plant mortality in either study. Bermudagrass injury after treatment with topramezone and tembotrione has not been described in detail.
Data describing the physiological effects of treating common bermudagrass with several rates of mesotrione, topramezone, and tembotrione are limited. Understanding carotenoid fluctuations after applications of mesotrione, topramezone, and tembotrione may provide valuable insight into improving bermudagrass control strategies with these herbicides. Thus, the objective of this study was to evaluate changes in common bermudagrass carotenoid pigments after treatment with mesotrione, topramezone, and tembotrione.
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