Interactions and effects on cysteine synthase activity of aminooxyacetate and boc-aminooxyacetate on the bioherbicides collectrotrichum truncatum and alternaria cassia and their weed hosts

Authors: Hoagland, Robert; HIRASE, KANGETSU - Mitsui Chemicals, Inc; Boyette, Clyde

Submitted to: American Journal of Plant Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/23/2021
Publication Date: 5/26/2021
Citation: Hoagland, R.E., Hirase, K., Boyette, C.D. 2021. Interactions and effects on cysteine synthase activity of aminooxyacetate and boc-aminooxyacetate on the bioherbicides collectrotrichum truncatum and alternaria cassia and their weed hosts. American Journal of Plant Sciences. https://doi.org/10.4236/ajps.2021.125052.
DOI: https://doi.org/10.4236/ajps.2021.125052

Interpretive Summary: Aminooxyacetate (AOA) exhibits phytotoxic and herbicidal activity attributed to its inhibition of enzymes that require pyridoxyl phosphate as a cofactor. Scientists from the USDA ARS Crop Production Systems research Unit and Biological Control of Pests Research Unit, Stoneville, MS, and Functional Chemicals Laboratory, Mitsui Chemicals, Japan have examined AOA and its analog, N-t-butoxycarbonyl-AOA (Boc-AOA) for phytotoxicity, interactions with weed pathogens (bioherbicides), and effects on an important pyridoxal requiring enzyme, cysteine synthase (CS). Hemp sesbania and sicklepod, and their fungal bioherbicides, (Colletotrichum truncatum and Alternaria cassiae, respectively) were examined. Phytotoxicity bioassays indicated that the bulky t-butoxycarbonyl moiety substitution on the AOA molecule did not substantially hinder expression of biological activity of Boc-AOA. Generally, spray application of the chemicals to dark-grown seedlings caused little growth effects, but root-feeding reduced stem elongation in both weeds. One positive interaction of the chemicals with these bioherbicides was the Boc-AOA:C. truncatum combination treatment on hemp sesbania. Both chemicals reduced extractable CS in seedlings by 30%, 72 h after treatment. CS activity was reduced by 15% in hemp sesbania treated with C. truncatum but increased 20% above control levels after infection of sicklepod by A. cassiae, suggesting CS may be involved in sicklepod defense mechanisms against this pathogen.

Technical Abstract: Aminooxyacetate (AOA) is a pyridoxal phosphate antagonist that inhibits various plant enzymes (including transaminases) which require pyridoxal phosphate as a cofactor and it exhibits phytotoxic and herbicidal properties. We examined AOA and its analog, N-t-butoxycarbonyl-AOA (Boc-AOA) for phytotoxicity, interactions with weed pathogens (bioherbicides), and effects on an important pyridoxal requiring enzyme, cysteine synthase (CS, E.C. 4.2.99.8). Studies were performed on two weeds, i.e., hemp sesbania [Sesbania exaltata (Raf.) Rybd. Ex A.W. Hill] and sicklepod (Senna obtusifolia), and two pathogens, (Colletotrichum truncatum and Alternaria cassiae), that are bioherbicidal agents against hemp sesbania and sicklepod, respectively. Pathogenicity tests, and assays for extractable, and in vitro CS activities were utilized. Phytotoxicity bioassays indicated that the bulky t-butoxycarbonyl moiety substitution on the AOA molecule did not substantially hinder expression of biological activity of Boc-AOA in these tests. Generally, spray application of the compounds to young dark-grown seedlings caused little growth effects, but root-feeding of the chemicals reduced growth (stem elongation) in both weeds. Hemp sesbania was generally more tolerant than sicklepod to these compounds. The only apparent positive interaction of the chemicals with these pathogens was the Boc-AOA:C. truncatum combination treatment on hemp sesbania. Both compounds reduced extractable CS in the seedlings by 30%, 72 h after treatment. CS activity was reduced by 15% in hemp sesbania treated with C. truncatum but increased 20% above control levels after infection of sicklepod by A. cassiae. This latter effect suggests that CS may be involved in sicklepod defense mechanisms against this pathogen.