Effect of herbicide diclofop‐methyl on proton extrusion from Lolium multiflorum seedlings differing in resistance and in fungal endophyte (Neotyphodium sp.) infection

Abstract

Lolium multiflorum (Italian ryegrass), an annual weed invading wheat and barley cropping systems, has evolved resistance to diclofop‐methyl (DM) herbicide. Earlier studies on the mode of action of DM in susceptible L. multiflorum and L. rigidum populations have shown that herbicide promotes oxidative stress leading to senescence, a process reversible through the action of auxins. The disruption of cell membrane potential (Em) appears to be correlated with DM phytotoxicity in susceptible populations, suggesting that the continuous H+ extrusion from plasmalemma to extracellular space is inhibited. L. multiflorum usually establishes a symbiotic relationship with fungal endophytes of the Neotyphodium genus. This fungus confers to host plants higher survival at sublethal dosages of DM, probably due to the production of auxinic compounds. Our goal was to characterize DM‐resistant and DM‐susceptible L. multiflorum populations infected (E+) and non‐infected (E−) with endophytes, by studying the capacity of H+ bumping of plasmalemma of intact roots under DM selection. We correlated the effects of DM on H+ disruption with plant survival. DM inhibited acidification markedly more in susceptible than in resistant populations. Continued extrusion of H+ by DM‐resistant cell membranes was positively related to plant survival and growth. There was no detectable difference in the capacity of bumping H+ between DM‐susceptible E+ and E− seedlings, even though survival was higher in E+ plants. The basis for the differential response in H+ extrusion between resistant and susceptible populations of L. multiflorum is discussed.

Impact of ozone on the viability and antioxidant content of grass seeds is affected by a vertically transmitted symbiotic fungus

“…Glutathione is a cytoplasmic and water soluble antioxidant proposed as a reliable marker of stress in orthodox seeds (Kranner et al, 2006;Seal et al, 2010), and our results show that glutathione can be affected by the endophyte, although a clear relationship with the viability of the fungus is not yet proven (Gundel et al, 2012b). Alternatively, the association of the endophyte to a higher level of some tocochromanol antioxidants (lipid-soluble and membrane-bound molecules) could explain the maintenance of membranes functionality in germinating seeds and the high survival of seedlings (Vila-Aiub et al, 2003;Gundel et al, 2012b). Additional experiments are needed in order to reveal the association of the endophyte presence with the role of the different antioxidants as well as the origin (i.e.…”

Weed resistance to acetyl coenzyme A carboxylase inhibitors: an update

“…Alternative modes of action proposed, such as the possibility that these herbicides are auxin antagonists that bind to putative cell membrane receptors to induce rapid depolarization of the membrane and cell death via oxidative damage (Ratterman and Balke 1988;Shimabukuro et al 2001), can thus be discounted. Although APPs and CHDs do depolarize cell membranes in vitro (e.g., Holtum et al 1994;Ratterman and Balke 1988;Vila-Aiub et al 2003), this might not occur in vivo at herbicide field rates. Depolarization of the cell membrane is very likely a secondary effect after ACC inhibition and the ensuing disruption of the fatty acid biosynthesis pathway, as has been proposed before (Di Tomaso 1994; Incledon and Hall 1997).…”

“…Recovery of transmembrane potential has been reported in several cases as a mechanism of resistance to ACC-inhibiting herbicides (Vila-Aiub et al 2003; for a review, see Holtum et al 1994) in the context of the hypothetical interaction of these herbicides with a putative binding site on cell membranes that was discussed in the section ''Structure and mode of action of ACC-inhibiting herbicides''. However, as discussed there, it seems more than likely that the membrane repolarization observed in some resistant plants is a secondary consequence of a resistance mechanism rather than the mechanism itself (Shukla et al 1997a).…”

Differential enantioselectivity of quizalofop ethyl and its acidic metabolite: Direct enantiomeric separation and assessment of multiple toxicological endpoints

“…In most cases, contaminant-modified membrane dysfunction such as varied membrane permeability is believed to be a first step, triggering membrane depolarization and inducing other toxicological actions including growth inhibition [27,28]. Initial changes of membrane permeability and subsequent depolarization, for example, occur both with diclofop methyl (DM) and diclofop acid (DA), analogues of QE and QA, respectively, and appear to be correlated with the phytotoxicity [15,40,41].…”