Herbicide diagnostics reveal multiple patterns of synthetic auxin resistance in kochia (Bassia scoparia)

Herbicide-resistant (HR) kochia is a growing problem in the Great Plains region of Canada and the United States (U.S.). Resistance to up to four herbicide sites of action, including photosystem II inhibitors, acetolactate synthase inhibitors, synthetic auxins, and the 5-enolpyruvylshikimate-3-phosphate synthase inhibitor glyphosate have been reported in many areas of this region. Despite being present in the U.S. since 1993/1994, auxinic-HR kochia is a recent and growing phenomenon in Canada. This study was designed to characterize (a) the level of resistance and (b) patterns of cross-resistance to dicamba and fluroxypyr in 12 putative auxinic-HR kochia populations from western Canada. The incidence of dicamba-resistant individuals ranged among populations from 0% to 85%, while fluroxypyr-resistant individuals ranged from 0% to 45%. In whole-plant dose-response bioassays, the populations exhibited up to 6.5-fold resistance to dicamba and up to 51.5-fold resistance to fluroxypyr based on visible injury 28 days after application. Based on plant survival estimates, the populations exhibited up to 3.7-fold resistance to dicamba and up to 72.5-fold resistance to fluroxypyr. Multiple patterns of synthetic auxin resistance were observed, where one population from Cypress County, Alberta was resistant to dicamba but not fluroxypyr, while another from Rocky View County, Alberta was resistant to fluroxypyr but not dicamba based on single-dose population screening and dose-response bioassays. These results suggest that multiple mechanisms may confer resistance to dicamba and/or fluroxypyr in Canadian kochia populations. Further research is warranted to determine these mechanisms. Farmers are urged to adopt proactive non-chemical weed management tools in an effort to preserve efficacy of the remaining herbicide options available for control of HR kochia.

A novel role for Cyclic Nucleotide-Gated Ion Channel 2 (DND1) in auxin signaling

ABSTRACTCyclic Nucleotide Gated Ion Channels (CNGCs) are non-selective cation channels that are involved in regulating responses to both biotic and abiotic stresses in plants. CNGC2 has been implicated in plant immunity and Ca2+ signaling through the study of the autoimmune phenotypes exhibited by the null mutant, defense, no death1 (dnd1). However, dnd1 also shows additional phenotypes that are unique among autoimmune mutants. This suggests that CNGC2 plays multiple biological roles beyond pathogen defense. In this study, we cloned the gene that encodes the first suppressor of dnd1 (cngc2), REPRESSOR OF DEFENSE, NO DEATH1 (RDD1), which encodes an auxin biosynthesis gene, YUCCA6 (YUC6). We found that dnd1 (cngc2) is defective in auxin-mediated root growth inhibition and gravitropic responses in roots. Consistently with these auxin resistance phenotypes, we found dnd1 shows a dampened response to exogenous auxin compared to wildtype plants using the auxin inducible DR5::GUS and DII:VENUS reporter systems. Finally, auxin-induced Ca2+ influx was examined using the Förster resonance energy transfer (FRET)-based, genetically encoded Ca2+ indicator yellow cameleon (YC)-Nano65. We captured severe defects in auxin-induced Ca2+ increase in dnd1. These defects were rescued by the rdd1 mutation. Our findings highlight the unexpected involvement of CNGC2 in auxin-induced Ca2+ signaling and calls into question the current interpretation of dnd1 phenotypes in defense signaling.

Occurrence and Molecular Characterization of Acetolactate Synthase (ALS) Inhibitor–Resistant Kochia (Kochia scoparia) in Western Canada

A survey of 109 fields was conducted across western Canada in spring 2007 to determine the extent of ALS-inhibitor and dicamba (synthetic auxin) resistance in kochia. Weed seedlings were collected from fields in three provinces of western Canada and transplanted into the greenhouse. Seeds were harvested from selfed plants, and the F1progeny were screened for resistance to the ALS-inhibitor mixture thifensulfuron–tribenuron or dicamba. All kochia populations were susceptible to dicamba. ALS inhibitor–resistant kochia was found in 85% of the fields surveyed in western Canada: 80 of 95 fields in Alberta, six of seven fields in Saskatchewan, and all seven fields in Manitoba. For the 93 ALS inhibitor–resistant populations, the mean frequency (±SE) of parental plants classified as resistant was 61 ± 3%. Most of the resistant populations (87%) were heterogeneous and contained both resistant and susceptible individuals.ALSsequence data (Pro197and Asp376mutations) and genotyping data (Trp574mutation) obtained for 87 kochia parental (i.e., field-collected) plants confirmed the presence of all three target-site mutations as well as two mutational combinations (Pro197+ Trp574, Asp376+ Trp574) in resistant individuals.

The SAR1 gene of Arabidopsis acts downstream of the AXR1 gene in auxin response

A screen for suppressors of the auxin resistant mutant axr1 in Arabidopsis thaliana has identified at least three second site suppressor loci called Suppressor of Auxin Resistance (SAR). In this study we focus on the SAR1 gene. Previous studies have documented the effects of the axr1 mutations on auxin-inhibition of root growth, auxin-induced gene expression, seedling morphology and aerial morphology. In this study, we show that the axr1 mutations also affect root hair development and epidermal cell length. The sar1-1 mutation suppresses at least partially, every aspect of the axr1 phenotype. Genetic experiments indicate that this suppression is gene specific. When crossed with the auxin-resistant mutant aux1-7, the suppressor has little affect on auxin response. However, the morphology of sar1-1 aux1-7 inflorescences is different from either of the single mutants indicating that both genes play a role in auxin mediated development of the inflorescence. The sar1-1 mutation also affects morphology in an AXR1 background. sar1-1 plants are shorter than wild-type, have altered leaf morphology, flower earlier than wild-type plants and appear to have reduced cell division in the primary root. In most respects sar1-1 axr1 and sar1 AXR1 plants are indistinguishable, indicating that sar1 both suppresses and is epistatic to axr1. Based on these results, we propose that SAR1 acts after AXR1 and that a major function of AXR1 is to relieve SAR1 mediated repression of auxin response.