Department of Crop, Soil, and Environmental Sciences, University of Arkansas, 1366 West Altheimer Drive, Fayetteville, Arkansas 72704, USA.
J Agric Food Chem. 2013 Jan 16;61(2):278-89. doi: 10.1021/jf304675j. Epub 2013 Jan 4.
Barnyardgrass biotypes from Arkansas (AR1 and AR2) and Mississippi (MS1) have evolved cross-resistance to imazamox, imazethapyr, and penoxsulam. Additionally, AR1 and MS1 have evolved cross-resistance to bispyribac-sodium. Studies were conducted to determine if resistance to acetolactate synthase (ALS)-inhibiting herbicides in these biotypes is target-site or non-target-site based. Sequencing and analysis of a 1701 base pair ALS coding sequence revealed Ala₁₂₂ to Val and Ala₁₂₂ to Thr substitutions in AR1 and AR2, respectively. The imazamox concentrations required for 50% inhibition of ALS enzyme activity in vitro of AR1 and AR2 were 2.0 and 5.8 times, respectively, greater than the susceptible biotype. Absorption of ¹⁴C-bispyribac-sodium, -imazamox, and -penoxsulam was similar in all biotypes. ¹⁴C-Penoxsulam translocation out of the treated leaf (≤2%) was similar among all biotypes. ¹⁴C-Bispyribac-treated AR1 and MS1 translocated 31- 43% less radioactivity to aboveground tissue below the treated leaf compared to the susceptible biotype. ¹⁴C-Imazamox-treated AR1 plants translocated 39% less radioactivity above the treated leaf and aboveground tissue below the treated leaf, and MS1 translocated 54 and 18% less radioactivity to aboveground tissue above and below the treated leaf, respectively, compared to the susceptible biotype. Phosphorimaging results further corroborated the above results. This study shows that altered target site is a mechanism of resistance to imazamox in AR2 and probably in AR1. Additionally, reduced translocation, which may be a result of metabolism, could contribute to imazamox and bispyribac-sodium resistance in AR1 and MS1.
阿肯色州（AR1 和 AR2）和密西西比州（MS1）的稗草生物型已对咪草烟、咪草酸和吡嘧磺隆产生了交叉抗性。此外，AR1 和 MS1 对双草醚也产生了交叉抗性。本研究旨在确定这些生物型对乙酰乳酸合成酶（ALS）抑制剂类除草剂的抗性是否基于靶标或非靶标。对 1701 个碱基对的 ALS 编码序列进行测序和分析，发现 AR1 和 AR2 中分别存在 Ala122Val 和 Ala122Thr 取代。AR1 和 AR2 中 ALS 酶活性的 50%抑制所需的咪草烟浓度分别比敏感生物型高 2.0 倍和 5.8 倍。所有生物型对 ¹⁴C-双草醚、-咪草烟和 -吡嘧磺隆的吸收相似。¹⁴C-吡嘧磺隆在处理叶片中的外排（≤2%）在所有生物型中相似。¹⁴C-双草醚处理的 AR1 和 MS1 与敏感生物型相比，向处理叶下方地上组织的转运活性减少了 31-43%。¹⁴C-咪草烟处理的 AR1 植株向处理叶上方和下方的地上组织的转运活性减少了 39%，MS1 植株向处理叶上方和下方的地上组织的转运活性分别减少了 54%和 18%，与敏感生物型相比。磷成像结果进一步证实了上述结果。本研究表明，靶标改变是 AR2 中咪草烟抗性的机制，可能也是 AR1 中咪草烟抗性的机制。此外，由于代谢作用导致的转运减少可能导致 AR1 和 MS1 对咪草烟和双草醚的抗性。
