This study investigates mechanisms of multiple resistance to glyphosate, acetyl-coenzyme A carboxylase (ACCase) and acetolactate synthase (ALS)-inhibiting herbicides in two Lolium rigidum populations from Australia. When treated with glyphosate, susceptible (S) plants accumulated 4- to 6-fold more shikimic acid than resistant (R) plants. The resistant plants did not have the known glyphosate resistance endowing mutation of 5-enolpyruvylshikimate-3 phosphate synthase (EPSPS) at Pro-106, nor was there over-expression of EPSPS in either of the R populations. However, [(14)C]-glyphosate translocation experiments showed that the R plants in both populations have altered glyphosate translocation patterns compared to the S plants. The R plants showed much less glyphosate translocation to untreated young leaves, but more to the treated leaf tip, than did the S plants. Sequencing of the carboxyl transferase domain of the plastidic ACCase gene revealed no resistance endowing amino acid substitutions in the two R populations, and the ALS in vitro inhibition assay demonstrated herbicide-sensitive ALS in the ALS R population (WALR70). By using the cytochrome P450 inhibitor malathion and amitrole with ALS and ACCase herbicides, respectively, we showed that malathion reverses chlorsulfuron resistance and amitrole reverses diclofop resistance in the R population examined. Therefore, we conclude that multiple glyphosate, ACCase and ALS herbicide resistance in the two R populations is due to the presence of distinct non-target site based resistance mechanisms for each herbicide. Glyphosate resistance is due to reduced rates of glyphosate translocation, and resistance to ACCase and ALS herbicides is likely due to enhanced herbicide metabolism involving different cytochrome P450 enzymes.

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It is demonstrated that individuals with different glyphosate resistance mechanisms can coexist in the same population, individuals from different populations may carry different resistance mechanisms and different mechanisms can act in concert within single E. colona plants. However, other plant factors or resistance mechanisms appear to modulate plant expression of EPSPS sensitivity to glyphosate.

Perhaps the most obvious phenotypes associated with chemical signaling between plants are manifested by parasitic species of Orobanchaceae. The development of haustoria, invasive root structures that allow hemiparasitic plants to transition from autotrophic to heterotrophic growth, is rapid, highly synchronous, and readily observed in vitro. Haustorium development is initiated in aseptic roots of the facultative parasite Triphysaria versicolor when exposed to phenolic molecules associated with host root exudates and rhizosphere bioactivity. Morphological features of early haustorium ontogeny include rapid cessation of root elongation, expansion, and differentiation of epidermal cells into haustorial hairs, and cortical cell expansion. These developmental processes were stimulated in aseptic T. versicolor seedlings by the application of exogenous phytohormones and inhibited by the application of hormone antagonists. Surgically dissected root tips formed haustoria if the root was exposed to haustorial-inducing factors prior to dissection. In contrast, root tips that were dissected prior to inducing-factor treatment were unable to form haustoria unless supplemented with indole-3-acetic acid. A transient transformation assay demonstrated that auxin and ethylene-responsive promoters were up-regulated when T. versicolor was exposed to either exogenous hormones or purified haustoria-inducing factors. These experiments demonstrate that localized auxin and ethylene accumulation are early events in haustorium development and that parasitic plants recruit established plant developmental mechanisms to realize parasite-specific functions.It has been estimated that over 4,000 species of angiosperms are able to directly invade and parasitize other plants (Nickrent, 2003). Parasitic plant species have widely different hosts and habits, ranging from mistletoes that grow on the tops of conifer trees to root parasites that live most of their lives underground (Press and Graves, 1995). A single feature common to all parasitic plants is the ability to develop invasive structures called haustoria (Riopel and Timko, 1995). After invasion, parasitic plant haustoria function as physiological bridges through which the parasite robs host plants of water and nutrients. The competence to form haustoria is the defining characteristic of parasitic plants, distinguishing them from epiphytic and mycoheterotrophic plants that either use host plants for physical support or associate via mycorrhizal intermediates (Kuijt, 1969;Leake, 1994).It is clear from several lines of evidence that parasitic plants evolved from nonparasitic autotrophs (Kuijt, 1969). There are two general models for the evolutionary origins of the haustoria that define plant parasitism. One model proposes that genes encoding haustorium development are foreign to plants and were introduced into parasitic species via an endosymbiotic or horizontal gene transfer event, perhaps from a haustorial-producing fungus or bacteria (Atsatt, 1973). An alterative hypothesis proposes that gen...

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The cowpea aphid (Aphis craccivora Koch) is considered a serious insect pest attacking several crops. We carried out biochemical studies to elucidate the role of the metabolising enzymes in conferring resistance to thiamethoxam, in two strains (resistant and susceptible) of the cowpea aphid. Bioassay experiments showed that the thiamethoxam selected strain developed a 48 fold resistance after consecutive selection with thiamethoxam for 12 generations. This resistant strain also exhibited cross-resistance to the tested carbamates; pirimicarb and carbosulfan, organophosphorus (malathion, fenitrothion, and chlorpyrifos-methyl), and the neonicotinoid (acetamiprid). Synergism studies have indicated that S,S,S-tributyl phosphorotrithioate (DEF), a known inhibitor for esterases, increased thiamethoxam toxicity 5.58 times in the resistant strain compared with the susceptible strain. Moreover, the biochemical determination revealed that carboxylestersae activity was 30 times greater in the resistant strain than in the susceptible strain. In addition, the enzyme activity of glutathione S-transferase (GST) and mixed function oxidases (mfo) increased only in the resistant strain 3.7 and 2.7 times, respectively, in relation to the susceptible (the control). Generally, our results suggest that the higher activity of the detoxifying enzymes, particularly carboxylesterase, in the resistant strain of the cowpea aphid, apparently have a significant role in endowing resistance to thiamethoxam, although additional mechanisms may contribute.

Determining the mechanisms of herbicide resistance in weeds allows for the development and implementation of applied management practices aimed to control and to prevent further spread of herbicide-resistant populations in crop fields. This research was conducted to determine propanil resistance and cross-resistance to other photosystem II (PSII) inhibitors in ricefield bulrush biotypes and to elucidate the mechanism of propanil resistance. To this end, propanil-resistant (R) and propanil-susceptible (S) biotypes were selected from field-collected populations after propanil spraying at the field rate, and whole-plant, dose–response experiments were conducted to evaluate cross-resistance to PSII inhibitors and interactions between propanil and the insecticides malathion and carbaryl. In addition, thepsbAgene from R and S biotypes was sequenced for amino acid alterations following polymerase chain reaction (PCR) amplification. Plant survival data indicated the R biotype displayed a 14-fold increase in propanil resistance relative to the susceptible (S) biotype. In addition, the propanil-R biotype also had increased resistance to the PSII-inhibitors bromoxynil, diuron, and metribuzin but was more susceptible to bentazon than were propanil-S plants. Synergism between propanil and the insecticides carbaryl and malathion was greater in the S biotype than it was in the R biotype, indicating that, unlike propanil resistance in weedy grasses, enhanced degradation of the herbicide molecule is not a mechanism of resistance for propanil in ricefield bulrush. A Val219to Ile substitution in the propanil-R chloroplast D1 protein was identified following sequencing of thepsbAgene. This research suggests a single-point mutation at the target site causes resistance to propanil, diuron, metribuzin, and bromoxynil but increasing susceptibility to bentazon in propanil-R ricefield bulrush, a novel Val219–Ile feature. To our knowledge, this is the first instance of propanil resistance in weeds because of a mechanism other than enhanced herbicide metabolism. Tank-mixing bentazon and propanil, where permitted, can control both propanil-R and propanil-S biotypes.

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