Aicklen Isabelle, Jugulam Mithila, Gaines Todd, Kramer William, Laforest Martin, Robinson Darren, Sikkema Peter, Tardif François
Department of Plant Agriculture University of Guelph Guelph Ontario Canada.
Department of Soil and Crop Sciences Texas A&M University College Station Texas USA.
Plant Direct. 2025 Sep 11;9(9):e70105. doi: 10.1002/pld3.70105. eCollection 2025 Sep.
Resistance to 2-methyl-4-chloro-phenoxyacetic acid (MCPA) was recently confirmed in a population of green pigweed () from Dresden, Ontario, Canada, with a resistance factor of 4.4. Resistance to synthetic auxin herbicides in species has previously been linked to non-target site resistance mechanisms with low-level resistance factors (< 10). Based on this information, an investigation into the mechanism of resistance to MCPA was conducted in this population of green pigweed. No significant differences in absorption, translocation, and metabolism of C-MCPA existed between the resistant and a susceptible population of green pigweed. An RNA-Sequencing experiment to identify differentially expressed genes also confirmed this result. Genes that were differentially expressed in the resistant population were linked to target site modifications. A single nucleotide polymorphism (SNP) conferring a leucine to phenylalanine substitution was identified in auxin response factor (ARF) 9. This mutation may be in the Phox and Bem1p (PB1) domain in ARF9, which facilitates the interaction between ARFs and Aux/IAA repressor proteins. The results demonstrate that the mechanism of resistance to MCPA is not a non-target site mechanism and may be linked to a target site modification. Specifically, a SNP in ARF9 could disrupt the interaction between ARF9 and other Aux/IAAs, which could prevent ubiquitination of Aux/IAAs and subsequent lethal action of MCPA.
最近在加拿大安大略省德累斯顿的一群绿猪草()中证实了对2-甲基-4-氯苯氧乙酸(MCPA)具有抗性,抗性因子为4.4。此前,物种对合成生长素除草剂的抗性与低水平抗性因子(<10)的非靶标位点抗性机制有关。基于此信息,对该绿猪草种群中MCPA的抗性机制进行了调查。抗性和敏感绿猪草种群之间在C-MCPA的吸收、转运和代谢方面没有显著差异。一项用于鉴定差异表达基因的RNA测序实验也证实了这一结果。在抗性种群中差异表达的基因与靶标位点修饰有关。在生长素响应因子(ARF)9中鉴定出一个导致亮氨酸向苯丙氨酸取代的单核苷酸多态性(SNP)。该突变可能位于ARF9的Phox和Bem1p(PB1)结构域中,该结构域促进了ARF与Aux/IAA阻遏蛋白之间的相互作用。结果表明,对MCPA的抗性机制不是非靶标位点机制,可能与靶标位点修饰有关。具体而言,ARF9中的一个SNP可能会破坏ARF9与其他Aux/IAA之间的相互作用,从而阻止Aux/IAA的泛素化以及MCPA随后的致死作用。