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Biology subjects

Mahey, M.

Publications and source records attributed to Mahey, M..

3 recordsLinked to original sources

Cell wall composition drives off-target sensitivity to indaziflam

Indaziflam is a potent alkylazine herbicide classified as a cellulose biosynthesis inhibitor (CBI) with broad-spectrum pre-emergence activity and long soil persistence. While its efficacy in commercial weed control is established, its off-target ecological footprint across taxa with non-cellulose cell wall compositions remains poorly defined. We evaluated the potential off-target biological impacts of indaziflam across organisms representing distinct cell wall architectures, including the yeast Saccharomyces cerevisiae (chitin/glucan), the unicellular alga Chlamydomonas reinhardtii (glycoprotein), and the early-diverging bryophyte Marchantia polymorpha (cellulose/hemicellulose/pectin). Indaziflam did not inhibit the growth of non-target organisms lacking plant-type cellulose cell walls. In S. cerevisiae, treatment unexpectedly accelerated growth rates to reach ED50 (12.95 h at 3200 pM vs. 16.23 h in control). Similarly, C. reinhardtii showed no growth suppression across concentration ranges up to 100 nM. Conversely, the non-vascular land plant M. polymorpha exhibited marked, dose-dependent sensitivity. In vitro, thallus surface area was significantly suppressed at concentrations above 1600 pM (p<0.05). In greenhouse trials, pre-emergence application of indaziflam at recommended (1X) and elevated (2X, 3X) field rates provided up to 100% control of liverwort establishment and biomass accumulation over an 8-week evaluation period. Off-target activity of indaziflam is strictly confined to land plants (Embryophytes) possessing conserved cellulose-containing cell walls, with no adverse growth effects observed in organisms featuring chitin- or glycoprotein-based wall structures. These findings clarify the selective environmental toxicity profile of indaziflam, demonstrating that its biological activity aligns closely with its CBI classification without causing widespread toxicity across non-plant soil organisms.

physiology↗

Investigating the mechanism of resistance to indaziflam in Poa annua

Indaziflam is an effective herbicide for controlling Poa annua, a weed, in turfgrass, orchards, and rangelands. An RNA-seq analysis was performed to identify differentially expressed genes associated with indaziflam-resistance in P. annua populations, with heterologous transformation performed for validation of candidate gene. Additionally, whole transcriptome variant calling was used to determine potential target site mutations. Transcriptome data were analyzed using weighted gene co-expression network analysis, Multiple modules were identified with high correlation to ED50 values of the resistant and susceptible populations. A cytochrome P450, CYP81A91_A, was identified that was homologous to CYP81A10 that confers resistance to five different herbicidal modes of action in Lolium rigidum. A single nucleotide polymorphism (SNP) causing an amino acid change (Thr432Arg) in coatomer subunit {gamma} was identified P. annua populations and several others originating from orchards. The up-regulated and positively correlated CYP81A91_A identified, when transformed to Arabidopsis thaliana, did not provide resistance to indaziflam; however, it did provide multifold resistance to simazine, another triazine class herbicide from a different MOA. A SNP in coatomer subunit {gamma} (Thr432Arg) was identified that may provide target site resistance given that coatomer proteins are involved in vesicle trafficking and in recycling of the cellulose synthase. HIGHLIGHTThis paper is a in-depth characterization of indaziflam resistance in Poa annua that identifies a novel mutation in coatomer subunit {gamma} as the potential root cause.

plant biology↗

Changes in cuticle composition co-regulate drought and herbicide resistance in horseweed (Erigeron canadensis)

Horseweed (Erigeron canadensis) is a widely distributed annual weed that can cause significant yield losses if not properly controlled. Its phenotypic plasticity allows it to rapidly acclimate to new environmental conditions, such as drought and herbicides, such as glyphosate, with the potential for cross stress acclimatization. The objectives of this research were to uncover the physiological and genetic effects at the intersection of drought stress and glyphosate resistance. To this end, we performed greenhouse dose response experiments, RNAseq, 14C glyphosate absorption and translocation, and cuticular lipid profiling via GC/MS. Greenhouse dose-response experiments revealed that, after drought stress, there was a 2.5-3.7 fold reduction in glyphosate sensitivity via a significant reduction in glyphosate absorption, regardless if the starting population was resistant or susceptible to the field use rate already. Cuticular waxes were collected from each population with and without drought stress and were analyzed via GC/MS. When comparing total wax loads of plants grown under WW and DS conditions, we found that drought stress significantly increased total wax loads for all three populations. Additionally drought stress substantial increases the proportion of triterpenoids in the cuticle. By RNAseq, we found serval triterpenoid biosynthesis genes upregulated after drought, which likely drive the changes in cuticle composition and ultimately increased glyphosate resistance following drought. Ultimately, understanding how drought impacts glyphosate resistance is critical for maintaining optimal weed control in the changing climate. HighlightDrought stress induces changes to cuticle composition and gene expression that reduce glyphosate absorption, thereby increasing horseweeds ability to survive glyphosate application.

physiology↗