Resistance to herbicides inhibiting acetolactate synthase (ALS) has been increasing at a faster rate than in any other herbicide group. The great majority of these cases are due to various single-nucleotide polymorphisms in the ALS gene endowing target site resistance. Many diagnostic techniques have been devised in order to confirm resistance and help producers to adopt the best management strategies. Recent advances in DNA technologies coupled with the knowledge of sequence information have allowed the development of accurate and rapid diagnostic tests. While whole plant-based diagnostic techniques such as seedling bioassays or enzyme-based in vitro bioassays provide accurate results, they tend to be labour- and/or space-intensive and will only respond to the particular herbicides tested, making resolution of cross-resistance patterns more difficult. Successful DNA-based diagnosis of ALS inhibitor resistance has been achieved with three main techniques, (1) restriction fragment length polymorphism, (2) polymerase chain reaction amplification of specific alleles and (3) denaturing high-performance liquid chromatography. All DNA-based techniques are relatively rapid and provide clear identification of the mutations causing resistance. Resistance based on non-target mechanisms is not identified by these DNA-based methods; however, given the prevalence of target site-based ALS inhibitor resistance, this is a minor inconvenience.

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Conditions and thresholds applied for evidence weighting of within-codon concordance (PM5) for pathogenicity vary widely between laboratories and expert groups. Because of the sparseness of available clinical classifications, there is little evidence for variation in practice. Methods: We used as a truthset 7541 dichotomous functional classifications of BRCA1 and MSH2, spanning 311 codons of BRCA1 and 918 codons of MSH2, generated from large-scale functional assays that have been shown to correlate excellently with clinical classifications. We assessed PM5 at 5 stringencies with incorporation of 8 in silico tools. For each analysis, we quantified a positive likelihood ratio (pLR, true positive rate/false positive rate), the predictive value of PM5-lookup in ClinVar compared with the functional truthset. Results: pLR was 16.3 (10.6-24.9) for variants for which there was exactly 1 additional colocated deleterious variant on ClinVar, and the variant under examination was equally or more damaging when analyzed using BLOSUM62. pLR was 71.5 (37.8-135.3) for variants for which there were 2 or more colocated deleterious ClinVar variants, and the variant under examination was equally or more damaging than at least 1 colocated variant when analyzed using BLOSUM62. Conclusion: These analyses support the graded use of PM5, with potential to use it at higher evidence weighting where more stringent criteria are met.

Trials were conducted over 2 years at three locations in Ontario to determine the tolerance of three sweet corn hybrids to postemergence application of nicosulfuron (25 and 50 g·ha–1), bromoxynil (280 and 560 g·ha–1), and nicosulfuron plus bromoxynil (25 + 280 g·ha–1 and 50 + 560 g·ha–1). All hybrids showed injury 7 days after treatment (DAT). The crop largely recovered from the injury in most treatments, as indicated by the ratings completed 14 and 28 DAT. However injury from the tankmix of nicosulfuron plus bromoxynil at both rates still appeared to be synergistic at 7, 14, and 28 DAT. Visual injury, height reductions and yield loss in the nicosulfuron plus bromoxynil (50 + 560 g·ha–1) treatment were more severe than in the other herbicide treatments. Yield of BSS5362 was significantly decreased in the nicosulfuron (50 g·ha–1) and nicosulfuron plus bromoxynil (50 + 560 g·ha–1) but was not affected by any other herbicide-hybrid combination. Caution must be exercised when using this tankmix combination, as there is potential to cause significant visual injury, height reductions and yield loss.