Norman M A, Liebl R A, Widholm J M
Department of Agronomy, University of Illinois, Urbana, Illinois 61801.
Plant Physiol. 1990 Oct;94(2):704-9. doi: 10.1104/pp.94.2.704.
Studies were conducted to determine the herbicidal site of clomazone action in tolerant-soybean (Glycine max [L.] Merr. cv Corsoy) (SB-M) and susceptible-cotton (Gossypium hirsutum [L.] cv Stoneville 825) (COT-M) photomixotrophic cell suspension cultures. Although a 10 micromolar clomazone treatment did not significantly reduce the terpene or mixed terpenoid content (microgram per gram fresh weight) of the SB-M cell line, there was over a 70% reduction in the chlorophyll (Chl), carotenoid (CAR), and plastoquinone (PQ) content of the COT-M cell line. The tocopherol (TOC) content was reduced only 35.6%. Reductions in the levels of Chl, CAR, TOC, and PQ indicate that the site of clomazone action in COT-M cells is prior to geranylgeranyl pyrophosphate (GGPP). The clomazone treatment did not significantly reduce the flow of [(14)C]mevalonate ([(14)C]MEV) (nanocuries per gram fresh weight) into CAR and the three mixed terpenoid compounds of SB-M cells. Conversely, [(14)C]MEV incorporation into CAR and the terpene moieties of Chl, PQ, and TOC in COT-M cells was reduced at least 73%, indicating that the site of clomazone action must be after MEV. Sequestration of clomazone away from the chloroplast cannot account for soybean tolerance to clomazone since chloroplasts isolated from both cell lines incubated with [(14)C]clomazone contained a similar amount of radioactivity (disintegrations per minute per microgram of Chl). The possible site(s) of clomazone inhibition include mevalonate kinase, phosphomevalonate kinase, pyrophosphomevalonate decarboxylase, isopentenyl pyrophosphate isomerase, and/or a prenyl transferase.
开展了多项研究,以确定异恶草酮在耐异恶草酮大豆(Glycine max [L.] Merr. cv Corsoy)(SB-M)和敏感棉花(Gossypium hirsutum [L.] cv Stoneville 825)(COT-M)光合自养细胞悬浮培养物中的除草作用位点。尽管10微摩尔异恶草酮处理并未显著降低SB-M细胞系中萜类或混合萜类化合物的含量(微克/克鲜重),但COT-M细胞系中的叶绿素(Chl)、类胡萝卜素(CAR)和质体醌(PQ)含量却降低了70%以上。生育酚(TOC)含量仅降低了35.6%。Chl、CAR、TOC和PQ水平的降低表明,异恶草酮在COT-M细胞中的作用位点在牻牛儿基牻牛儿基焦磷酸(GGPP)之前。异恶草酮处理并未显著降低[(14)C]甲羟戊酸([(14)C]MEV)(纳居里/克鲜重)流入SB-M细胞中CAR和三种混合萜类化合物的流量。相反,COT-M细胞中[(14)C]MEV掺入CAR以及Chl、PQ和TOC的萜类部分至少降低了73%,这表明异恶草酮的作用位点一定在MEV之后。异恶草酮与叶绿体隔离并不能解释大豆对异恶草酮的耐受性,因为从用[(14)C]异恶草酮孵育的两种细胞系中分离出的叶绿体含有相似量的放射性(每微克Chl每分钟的衰变数)。异恶草酮抑制的可能位点包括甲羟戊酸激酶、磷酸甲羟戊酸激酶、焦磷酸甲羟戊酸脱羧酶、异戊烯基焦磷酸异构酶和/或异戊烯基转移酶。