Herbicide multiple‐resistance in a Lolium rigidum biotype is endowed by multiple mechanisms: isolation of a subset with resistant acetyl‐CoA carboxylase

Abstract

The development of herbicide multiple‐resistance in weed species represents a major threat to current agricultural practices. The mechanistic basis for herbicide multiple‐resistance has been investigated in a population of the annual grass weed Lolium rigidum Gaud. (annual ryegrass) resistant to herbicides affecting 6 target sites. A subset of the resistant population (R2 subset) has been isolated by germination on a medium containing the acetyl‐CoA carboxylase (ACCase, EC 6.4.1.2) inhibiting herbicide, sethoxydim ((2‐[1‐(ethoxyimino)butyl]‐5‐[2‐(ethylthio)propyl]‐3‐hydroxy‐2‐cyclohexen‐1‐one)). This 12% R2 subset of the population is 600 times more resistant to sethoxydim and between 30 to 200 times more resistant to other ACCase inhibitors than the bulk of the R population. The subset has a form of ACCase which is 6 to 55 times less sensitive to inhibition by these herbicides than the enzyme present in the bulk of the resistant or in the susceptible population. There was no difference in the uptake and metabolic degradation of [4‐14C]sethoxydim between the R2 subset and the unselected R population. These results show the accumulation of different resistance mechanisms in that single population. Furthermore we propose that this accumulation of multiple resistance mechanisms is the basis for herbicide multiple‐resistance in this biotype.

The molecular bases for resistance to acetyl co-enzyme A carboxylase (ACCase) inhibiting herbicides in two target-based resistant biotypes of annual ryegrass (Lolium rigidum)

“…Therefore, the search for mutations endowing ACCase herbicide resistance is conducted by examining the CT domain of the plastidic ACCase gene. In this study, with two L. rigidum biotypes in which the resistance is known to be due to a resistant ACCase (Tardif et al 1993;Tardif and Powles 1994), the CT domain sequences of the plastidic ACCase gene were analyzed and compared to a known susceptible biotype. In a total of 107 individual resistant plants examined (Table 5) every resistant plant displayed an Ile-to-Leu amino acid substitution at amino acid-127 (amino acid-1780 of plastidic ACCase in S. viridis or À1781 in A. myosuroides).…”

“…In contrast, the SLR 31 biotype displays multiple resistances across several herbicide modes of action, including resistance to the ACCase herbicides (Powles and Matthews 1992). Importantly, approximately 12% of the SLR 31 population is resistant to certain APP and CHD herbicides due to a resistant ACCase (Tardif and Powles 1994). This ACCase resistant subset is referred to as SLR 31-R2 and only this ACCase target-based resistant subset of the multiple resistant population SLR 31 was used in the experiments reported here.…”

“…In this contribution we have examined L. rigidum biotypes resistant to ACCase inhibiting herbicides due to a herbicide resistant ACCase enzyme. We have compared two resistant biotypes (known as SLR3 and SLR31-R2) that are geographically distinct but exhibit similar patterns of cross-resistance to ACCase herbicides at the whole plant and at the ACCase enzyme level (Tardif et al 1993;Tardif and Powles 1994). Here, we demonstrate that amino acid substitutions in ACCase, due to nucleotide substitutions in the CT domain of the plastidic ACCase gene, are linked with resistance to herbicides in these two resistant ryegrass biotypes.…”

Distribution and frequency of herbicide-resistant wild oat (Avena spp.) across the Western Australian grain belt

“…For diclofop-methyl, all surviving seedlings were cut back to a height of 30 mm at 21 days after treatment, allowed to regrow for 5 days, and then treated with the cyclohexanedione ACCase-inhibiting herbicide sethoxydim (Table 2). Sethoxydim was applied to diclofop-methyl survivors because previous work has shown that plants can metabolise diclofop-methyl but not sethoxydim (Tardif and Powles 1994), indicating target site resistance in the plants which survived both herbicide treatments. All ACCase and ALS-inhibiting herbicides were applied at the 2-3 leaf stage and plants were assessed for mortality 21 days after treatment.…”

“…Plants are generally not able to metabolise sethoxydim, therefore resistance to this herbicide is likely due to target-site ACCase gene mutation(s) (Tardif and Powles 1994). Of the 103 populations assessed as diclofop-methyl-resistant or developing resistance, only 12 (12%) of these populations were classified as resistant to sethoxydim, with another 12 populations in the developing resistance category (Table 3).…”