Rapid photosynthetic and physiological response of 2,4-D–resistant Sumatran fleabane (Conyza sumatrensis) to 2,4-D as a survival strategy

Abstract

In this work, we evaluated the short time-induced oxidative stress-mediated rapid metabolic and physiological responses of resistant and susceptible Sumatran fleabane [Conyza sumatrensis (Retz.) E. Walker; syn.: Erigeron sumatrensis Retz.] to 2,4-D herbicide. Fixed conditions (25 °C and 65 ±5% relative humidity), we assayed injury symptoms, chlorophyll a fluorescence and antioxidative systems of both resistant and susceptible biotypes to 2,4-D (1005 g a.e. ha-1). Under 15°C vs 25°C temperatures and light and dark conditions, oxidative stress-mediated damage was assayed on plants that received 2,4-D herbicide applications. The injury symptoms observed in the 2,4-D resistant biotype were rapid necrosis in leaves within 30 min, with the re-establishment of normal growth within 1- to 2-weeks after 2,4-D treatment. The basal antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) in the resistant biotype were greater than to the susceptible, though the activities of all enzymes generally did not differ between untreated and treated in the resistant biotype. The resistant biotype showed great reduction (at 1 and 4 h after application) in the photosynthetic electron transport chain performance index, while in the susceptible biotype these metabolic changes were detected only after 4 h. The resistant biotype recovered from the foliar damage 1- to 2-weeks after 2,4-D application, while the susceptible biotype was controlled. The production of H2O2 was responsive to temperature and increased faster in the 2,4-D-resistant biotype than in the susceptible one at both 15°C and 25°C; however, there was a greater increase at 25°C in the resistant biotype. The H2O2 production was not light-dependent in 2,4-D-resistant C. sumatrensis, with increases even under dark conditions. The 2,4-D resistant biotype showed rapid photosynthetic damage, possibly due to the rapid necrosis and leaf disruption, and increased the H2O2 content compared to the susceptible biotype.

Rapid necrosis: Implications of environmental conditions and plant growth stage on 2,4-D resistance and effect of other auxinic herbicides in Sumatran fleabane (Conyza sumatrensis)

“…A previous study indicated that under low light (29 µmol m –2 s –1 ), H 2 O 2 production was reduced in Sumatran fleabane and the onset of RN symptoms was delayed in comparison to high-light conditions (848 µmol m –2 s –1 ) (Queiroz et al 2020). A similar response was observed in another 2,4-D-resistant biotype of Sumatran fleabane, which showed similar levels of H 2 O 2 under dark and under light (520 µmol m –2 s –1 ) conditions, and it was higher in the resistant biotype than in the susceptible biotype (Leal et al 2022). Another factor affecting the onset of RN is the plant growth stage in the timing of herbicide spraying, which is variable in field conditions.…”

“…After 4 h of treatment, these metabolic alterations were also observed in the susceptible biotype. Photosynthetic damage was rapidly observed in the resistant compared with the susceptible biotype due to the differential physiological response to 2,4-D (Leal et al 2022). These symptoms are probably related to the increase of ROS and the effect of the necrosis of the leaf tissue on photosynthesis.…”

“…Recently, a second study on this case of resistance identified that the RN mechanism may be related to changes in auxin transport or the transport inhibitor response 1 receptor and not related to 2,4-D detoxification by glutathione-S-transferase or cytochrome P450 monooxygenase enzymes (Queiroz et al 2022). Furthermore, the oxidative stress related to RN was responsive to temperature and was not light-dependent in Sumatran fleabane resistant plants that also showed rapid photosynthetic damage (Leal et al 2022). There is no report of other species showing similar resistance to auxinic herbicides in the literature (Figueiredo et al 2022; Peterson et al 2016).…”

Identification of a Novel 2,4-D Metabolic Detoxification Pathway in 2,4-D-Resistant Waterhemp (Amaranthus tuberculatus)

“…24,25 Nontarget site resistance mechanisms reported for synthetic auxin herbicides include reduced herbicide translocation 26−28 and rapid response cell death following 2,4-D treatment. 29,30 Metabolism-based resistance to synthetic auxin herbicides was reported for MCPA (2-methyl-4-chlorophenoxyacetic acid)-resistant hemp nettle (Galeopsis tetrahit), 31 mecopropresistant chickweed (Stellaria media), 32 2,4-D-resistant corn poppy (Papaver rhoeas), 33,34 2,4-D-resistant waterhemp, 18,35,36 and 2,4-D-resistant Palmer amaranth (Amaranthus palmeri) 37 in which 2,4-D was metabolized 20−30% faster than in susceptible plants. 2,4-D metabolites have been characterized in susceptible weed species.…”

“…Many cases of synthetic auxin herbicide resistance have been reported in weeds, and yet, most of the biochemical mechanisms regulating these phenotypes are still unknown. , Two examples of target site mutations in Aux/IAA (auxin/indole-3-acetic acid) coreceptor genes that cause synthetic auxin herbicide resistance were recently identified. , Nontarget site resistance mechanisms reported for synthetic auxin herbicides include reduced herbicide translocation − and rapid response cell death following 2,4-D treatment. , Metabolism-based resistance to synthetic auxin herbicides was reported for MCPA (2-methyl-4-chlorophenoxyacetic acid)-resistant hemp nettle (Galeopsis tetrahit), mecoprop-resistant chickweed (Stellaria media), 2,4-D-resistant corn poppy (Papaver rhoeas), , 2,4-D-resistant waterhemp, ,, and 2,4-D-resistant Palmer amaranth (Amaranthus palmeri) in which 2,4-D was metabolized 20–30% faster than in susceptible plants. 2,4-D metabolites have been characterized in susceptible weed species .…”