Increased glutathione conjugation of atrazine confers resistance in a Wisconsin velvetleaf (Abutilon theophrasti) biotype
Increased glutathione conjugation of atrazine confers resistance in a Wisconsin velvetleaf (Abutilon theophrasti) biotype
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DOI：
10.1006/pest.1996.0045
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发表时间：
1996-07-01
影响因子：
4.7
通讯作者：
Stoltenberg, DE
中科院分区：
文献类型：
--
作者：
Gray, JA;Balke, NE;Stoltenberg, DE
进行实验以确定威斯康星苘麻生物型 (WRB1) 对莠去津 (2-氯-4-乙氨基-6-异丙氨基-s-三嗪) 的抗性机制，并确定是否相同的机制导致马里兰苘麻生物型 (MRB) 对莠去津的抗性。阿特拉津同样抑制 WRB1 的分离类囊体和威斯康星州阿特拉津敏感的绒叶种质 (WSA1) 的光合电子传递，这表明阿特拉津抗性机制并不是光系统 II 中阿特拉津作用的不太敏感位点。在 12 小时的时间过程中，WRB1 和 WSA1 幼苗对水培 [C-14]莠去津或营养液的吸收没有差异，但 WRB1 中莠去津的吸收高于 MRB。在阿特拉津暴露 6 小时和 12 小时时，WRB1 茎中的放射性浓度高于 WSA1 茎，但在暴露 12 小时时，WRB1 中的放射性浓度低于 WSA1 叶。这些结果表明莠去津向叶片的易位减少是 WRB1 抗性机制的一个因素。 WSA1、WRB1 和 MRB 是一种通过谷胱甘肽结合和 N-脱烷基作用代谢的莠去津，并产生不可萃取的残留物。与WSA1相比，WRB1和MRB在茎和叶中代谢更多的莠去津。两种抗性生物型中的主要可提取代谢物是谷胱甘肽、L-半胱氨酸和莠去津的 N-乙酰基-L-半胱氨酸缀合物，这些代谢物是在谷胱甘肽缀合途径中产生的。在阿特拉津暴露 6 小时和 12 小时时，WRB1 茎中不可萃取残留物的浓度均高于 WSA1 茎。因此，莠去津代谢增加是WRB1对莠去津耐药的主要因素。此外，考虑到MRB比WRB1对莠去津的吸收较低，WRB1和MRB中莠去津的代谢在定性和定量上相似。因此，这两种地理上孤立的绒叶生物型的抗性是由于莠去津的谷胱甘肽缀合增加所致。 (C) 1996 学术出版社
Experiments were conducted to determine the mechanism of resistance to atrazine (2-chloro-4-ethylamino-6-isopropylamino-s-triazine) in a Wisconsin velvetleaf (Abutilon theophrasti Medicus) biotype (WRB1) and to determine if the same mechanism is responsible for atrazine resistance in a Maryland velvetleaf biotype (MRB). Atrazine equally inhibited photosynthetic electron transport by isolated thylakoids of WRB1 and a Wisconsin atrazine-susceptible velvetleaf accession (WSA1), suggesting that the mechanism of atrazine resistance is not a less-sensitive site of atrazine action in photosystem II. WRB1 and WSA1 seedlings did not differ in uptake of hydroponically fed [C-14]atrazine or nutrient solution over a 12-hr time course, but atrazine uptake was greater in WRB1 than MRB. Concentration of radioactivity was greater in WRB1 than WSA1 stems at both 6 and 12 hr of atrazine exposure, but was less in WRB1 than WSA1 leaves at 12 hr of exposure. These results suggest that decreased translocation of atrazine to leaves is a factor in the mechanism of resistance in WRB1. WSA1, WRB1, and MRB an metabolized atrazine via glutathione conjugation and N-dealkylation, as well as producing nonextractable residues. Compared to WSA1, both WRB1 and MRB metabolized more atrazine in stems and leaves. Predominant extractable metabolites in the two resistant biotypes were the glutathione, L-cysteine, and N-acetyl-L-cysteine conjugates of atrazine, metabolites produced in the glutathione conjugation pathway. Concentration of nonextractable residues was greater in WRB1 than WSA1 stems at both 6 and 12 hr of atrazine exposure. Thus, increased atrazine metabolism was the major factor accounting for WRB1 resistance to atrazine. Furthermore, in WRB1 and MRB, atrazine metabolism was qualitatively and quantitatively similar, after consideration of the lower atrazine uptake by MRB than WRB1. Hence, resistance in both of these geographically isolated velvetleaf biotypes results from increased glutathione conjugation of atrazine. (C) 1996 Academic Press