Characterizing the Auxin Herbicide Response in Horseweed ( Erigeron canadensis)
Auxin herbicides such as 2,4-D and dicamba have been used for over 70 years to control problematic broadleaf weed species. The auxin herbicide mode of action, particularly the precise mechanism in which auxin herbicides initiate the cascade of physiological effects that results in plant death, has yet to be fully characterized. As novel auxin herbicides are commercialized, it is important to understand the activity of new actives in relation to older chemistry. The first objective of this research was to evaluate the value of halauxifen-methyl, a new arylpicolinate auxin compound, against current auxin standards to manage glyphosate-resistant horseweed (Erigeron canadensis). The second objective was to employ a transcriptomic approach and utilize classic physiology to investigate the auxin herbicide mode of action. In field efficacy studies, halauxifen-methyl consistently controlled horseweed up to 19 cm in height. A comparable field use rate of dicamba controlled horseweed up to 17 cm in height while 2,4-D failed to control horseweed of any height. Greenhouse and agar-based root inhibition assays confirmed observations made in the field. These results indicate that halauxifen-methyl has the potential to manage horseweed with equivalent or greater control than other current auxin herbicide standards. Within 1 hour of treatment (HAT), 48 genes were consistently upregulated across the three herbicides, many of which are involved in the auxin-activated signaling pathway and general auxin response. The enzyme involved in the rate-limiting step of ABA biosynthesis, NCED, was upregulated in all herbicide treatments at 1 and 6 HAT. Increased ABA concentration in leaf tissue at 6 HAT supported RNA-seq results. Interestingly, auxin herbicides directly upregulated NCED expression and ABA accumulation in a manner independent from ethylene biosynthesis as previously suggested. These results provide novel evidence that ABA, but not necessarily ethylene, is a key player in initial auxin herbicide mode of action. At 6 HAT, 735 genes were upregulated by all herbicide treatments; these genes were associated with hormone signaling, metabolism, and gene expression. The GO terms representing the 501 genes downregulated in all herbicide treatments were broadly categorized under photosynthesis. At 6 HAT, over 50% of the genes differentially expressed among the three herbicide treatments were unique to a single active ingredient. While there are an abundance of transcriptome similarities induced by each herbicide that account for the general auxin herbicide response, distinct gene expression changes exclusive to each compound cannot be ignored as a contributor to the mode of action. Future research should include a fine-tuned pathway analysis and identification of key genes involved in upstream transcriptome regulation in horseweed to further differentiate auxin herbicide action by active ingredient. Overall, the interdisciplinary nature of the research presented in this dissertation provides valuable insight on the action of auxin herbicides on horseweed.
Young, Purdue University.
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