Populations of rigid ryegrass with resistance to glyphosate have started to become a problem on fence lines of cropping fields of southern Australian farms. Seed of rigid ryegrass plants that survived glyphosate application were collected from two fence line locations in Clare, South Australia. Dose–response experiments confirmed resistance of these fence line populations to glyphosate. Both populations required 9- to 15-fold higher glyphosate dose to achieve 50% mortality in comparison to a standard susceptible population. The mechanism of resistance in these populations was investigated. Sequencing a conserved region of the gene encoding 5-enolpyruvyl-shikimate-3-phosphate synthase identified no differences between the resistant and susceptible populations. Absorption of glyphosate into leaves of the resistant populations was not different from the susceptible population. However, the resistant plants retained significantly more herbicide in the treated leaf blades than did the susceptible plants. Conversely, susceptible plants translocated significantly more herbicide to the leaf sheaths and untreated leaves than the resistant plants. The differences in translocation pattern for glyphosate between the resistant and susceptible populations of rigid ryegrass suggest resistance is associated with altered translocation of glyphosate in the fence line populations.

A suspected glyphosate-resistant (R) junglerice population was collected from a glyphosate-R corn field near Durham in northern California where glyphosate had been applied at least twice a year for over 6 yr. Based on the amount of glyphosate required to reduce growth by 50% (ED50), the R population was 6.6 times more R than the susceptible (S) standard population. Based on the glyphosate concentration that inhibits EPSPS by 50% based on shikimate accumulation (I50) in leaf discs, R plants were four times more R than S plants. By 3 d after treatment with 0.42 kg ae ha−1 glyphosate, the S population had accumulated approximately five times more shikimate than the R population. No differences in [14C]-glyphosate uptake and translocation were detected between R and S plants. However, partial sequencing of the EPSPS gene revealed a mutation in R plants causing a proline to serine change at EPSPS position 106 (P106S). Our results reveal the first case of a P106S target site mutation associated with glyphosate resistance in junglerice.

Glyphosate resistance was first discovered in populations of rigid ryegrass in Australia in 1996. Since then, glyphosate resistance has been detected in additional populations of rigid ryegrass and Italian ryegrass in several other countries. Glyphosate-resistant rigid ryegrass and Italian ryegrass have been selected in situations where there is an overreliance on glyphosate to the exclusion of other weed control tactics. Two major mechanisms of glyphosate resistance have been discovered in these two species: a change in the pattern of glyphosate translocation such that glyphosate accumulates in the leaf tips of resistant plants instead of in the shoot meristem; and amino acid substitutions at Pro 106 within the target site, 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS). There are also populations with both mechanisms. In the case of glyphosate resistance, the target site mutations tend to provide a lower level of resistance than does the altered translocation mechanism. Each of these resistance mechanisms is inherited as a single gene trait that is largely dominant. As these ryegrass species are obligate outcrossers, this ensures resistance alleles can move in both pollen and seed. Some glyphosate-resistant rigid ryegrass populations appear to have a significant fitness penalty associated with the resistance allele. Field surveys show that strategies vary in their ability to reduce the frequency of glyphosate resistance in populations and weed population size, with integrated strategies—including alternative weed management and controlling seed set of surviving plants—the most effective.