Influence of multiple herbicide resistance on growth in Amaranthus tuberculatus

Plant defence traits, such as herbicide resistance mutations, may incur a fitness cost to plants that become evident when the trait is not needed. However, individuals with multiple herbicide resistance traits may decrease fitness beyond that of plants with a single herbicide resistance mutation. Multiple herbicide‐resistant (MHR) Amaranthus tuberculatus populations are becoming more prevalent in Midwest United States agroecosystems. The objective was to determine whether selected MHR A. tuberculatus populations express differential development when grown in a herbicide‐free environment. The hypothesis was that MHR A. tuberculatus populations become increasingly less fit when additional herbicide resistances evolve. Multiple herbicide‐resistant and herbicide‐susceptible A. tuberculatus populations were grown in a herbicide‐free field for 20 weeks for two seasons. Differences (P < 0.001) in apical growth were detected 5 and 7 weeks after transplanting for all populations in 2016 and 2017 respectively. Gender and population influenced (P < 0.001) flowering date, with males flowering up to 1.5 weeks earlier than females, but did not cause pollination asynchrony. Shoot biomass was not different (P = 0.84) across A. tuberculatus populations, but there were differences (P < 0.001) for gender and year. Seed production was different amongst A. tuberculatus populations (P = 0.001), but was not influenced by the number of MHR traits. Conversely, a negative quadratic relationship between seed mass and the number of MHR traits was observed (r² = 0.32; P < 0.001). The experiment results demonstrate that MHR in A. tuberculatus populations is not incurring a fitness penalty that will remove the populations in the immediate future.     

Triazine resistance in Amaranthus tuberculatus (Moq) Sauer that is not site-of-action mediated

While surveying Illinois Amaranthus tuberculatus (Moq) Sauer (tall waterhemp) half-sib populations for herbicide response variability, several were observed to segregate for resistance to atrazine. Studies were conducted on greenhouse-grown A tuberculatus plants to compare atrazine responses among populations that were segregating for resistance (SegR), uniformly sensitive (UniS) or uniformly resistant (UniR). In chlorophyll fluorescence assays, leaves of plants from the SegR and UniS populations displayed changes in fluorescence after treatment with atrazine, indicating that atrazine was inhibiting electron transport of photosystem II in chloroplasts. Sequencing of a fragment of psbA, which encodes the D1 protein, revealed that the SegR population did not contain the amino acid substitution that is typically found in triazine-resistant plants. Whole-plant herbicide dose-response experiments revealed that, relative to the UniS population, atrazine resistances in the UniR and SegR populations were > 770-fold and 16-fold, respectively. The SegR population was also resistant to cyanazine (59-fold), but not to metribuzin, linuron or pyridate. Triazine resistance in the SegR population was shown to be a nuclear inherited trait, unlike maternal inheritance of site-of-action mediated triazine resistance found in the UniR population. Taken collectively, these findings confirm the existence of two distinct triazine resistance mechanisms in A tuberculatus.     

Amaranthus palmeri resistance and differential tolerance of Amaranthus palmeri and Amaranthus hybridus to ALS-inhibitor herbicides

Suspected imazaquin-resistant accessions of Amaranthus palmeri were studied to determine the magnitude of resistance and cross-resistance to acetolactate synthase (ALS)-inhibiting herbicides and compare differential tolerance of A palmeri and Amaranthus hybridus to ALS inhibitors. Five of seven A palmeri accessions were resistant to imazaquin. The most imazaquin-resistant accession, accession 7, also showed 74, 39 and 117 times higher resistance than the susceptible biotype to chlorimuron, diclosulam and pyrithiobac, respectively. Resistance to imazaquin and cross-resistance to other ALS inhibitors in A palmeri was due to a less-sensitive ALS enzyme. A palmeri was 70 times more tolerant to imazaquin than A hybridus. A palmeri was also seven times more tolerant to pyrithiobac than A hybridus. Differences in ALS enzyme sensitivity could not fully account for the high tolerance of A palmeri to imazaquin compared to A hybridus. Both species were equally affected by chlorimuron and diclosulam.     

Resistance to HPPD-inhibiting herbicides in a population of waterhemp (Amaranthus tuberculatus) from Illinois, United States

BACKGROUND: A population of waterhemp in a seed maize production field in central Illinois, United States, was not adequately controlled after post‐emergence applications of herbicides that inhibit 4‐hydroxyphenylpyruvate dioxygenase (HPPD). RESULTS: Progeny from the field population survived following treatment with mesotrione, tembotrione or topramezone applied to the foliage either alone or in combination with atrazine in greenhouse experiments. Dose–response experiments indicated that the level of resistance to the HPPD inhibitor mesotrione is at least tenfold relative to sensitive biotypes. CONCLUSION: These studies confirm that waterhemp has evolved resistance to HPPD‐inhibiting herbicides. Copyright © 2011 Society of Chemical Industry     

Evolving understanding of the evolution of herbicide resistance

A greater number of, and more varied, modes of resistance have evolved in weeds than in other pests because the usage of herbicides is far more extensive than the usage of other pesticides, and because weed seed output is so great. The discovery and development of selective herbicides are more problematic than those of insecticides and fungicides, as these must only differentiate between plant and insect or pathogen. Herbicides are typically selective between plants, meaning that before deployment there are already some crops possessing natural herbicide resistance that weeds could evolve. The concepts of the evolution of resistance and the mechanisms of delaying resistance have evolved as nature has continually evolved new types of resistance. Major gene target‐site mutations were the first types to evolve, with initial consideration devoted mainly to them, but slowly ‘creeping’ resistance, gradually accruing increasing levels of resistance, has become a major force owing to an incremental accumulation of genetic changes in weed populations. Weeds have evolved mechanisms unknown even in antibiotic as well as other drug and pesticide resistances. It is even possible that cases of epigenetic ‘remembered’ resistances may have appeared. Copyright © 2009 Society of Chemical Industry     

Molecular characterisation of resistance to ALS-inhibiting herbicides in Hordeum leporinum biotypes

BACKGROUND: The acetolactate synthase (ALS)-inhibiting herbicide sulfosulfuron is registered in Australia for the selective control of Hordeum leporinum Link. in wheat crops. This herbicide failed to control H. leporinum on two farms in Western Australia on its first use. This study aimed to determine the level of resistance of three H. leporinum biotypes, identify the biochemical and molecular basis and develop molecular markers for diagnostic analysis of the resistance. RESULTS: Dose-response studies revealed very high level (>340-fold) resistance to the sulfonylurea herbicides sulfosulfuron and sulfometuron. In vitro ALS assays revealed that resistance was due to reduced sensitivity of the ALS enzyme to herbicide inhibition. This altered ALS sensitivity in the resistant biotypes was found to be due to a mutation in the ALS gene resulting in amino acid proline to serine substitution at position 197. In addition, two- to threefold higher ALS activities were consistently found in the resistant biotypes, compared with the known susceptible biotype. Two cleaved amplified polymorphic sequence (CAPS) markers were developed for diagnostic testing of the resistant populations. CONCLUSION: This study established the first documented case of evolved ALS inhibitor resistance in H. leporinum and revealed that the molecular basis of resistance is due to a Pro to Ser mutation in the ALS gene.     

Herbicide safeners: a review

Herbicide safeners selectively protect crop plants from herbicide damage without reducing activity in target weed species. This paper provides an outline of the discovery and uses of these compounds, before reviewing literature devoted to defining the biochemical and physiological mechanisms involved in safener activity. Emphasis is placed on the effects of safeners on herbicide metabolism and their interactions with enzyme systems, such as cytochrome P₄₅₀ mono-oxygenases and glutathione-S-transferases. Attention is drawn to the potential wide-ranging applications of safeners and, in particular, their use as powerful research tools with which to identify and manipulate those mechanisms which contribute to herbicide selectivity and resistance. © 1999 Society of Chemical Industry