Intact spinach chloroplasts were used to determine if clomazone, 5-OH clomazone, and/or 5-keto clomazone inhibited the chloroplastic isoprenoid pathway. When isopentenyl pyrophosphate was used as a precursor, neither clomazone nor the clomazone metabolites (5-OH clomazone and 5-keto clomazone) inhibited the formation of products separated by HPLC in the organic phase. However, when pyruvate, a substrate for the first committed step of the pathway, was used as a precursor, both 5-keto clomazone and fosmidomycin reduced the formation of a non-polar product and increased the formation of a polar product in the organic phase. Only 5-keto clomazone, not 5-OH clomazone or clomazone, inhibited the formation of an additional product other than fosmidomycin in the aqueous phase from pyruvate incorporation. In an in vitro assay, 5-keto clomazone inhibited DXP synthase, the enzyme catalyzing the first committed step of the chloroplastic isoprenoid pathway. Therefore, our studies show that neither clomazone nor 5-OH clomazone inhibits the chloroplastic isoprenoid pathway, only 5-keto clomazone does.
|Number of pages||8|
|Journal||Pesticide Biochemistry and Physiology|
|State||Published - May 2006|
Bibliographical noteFunding Information:
The authors thank Dr. Marc Clastre from the Laboratoire de Biologie Moleculaire et Biochimie Vegetale, Faculte de Pharmacie for providing the construct expressing C. roseus DXP synthase (XL1-blue/TCRDXS). This work was supported by the Higher Education Council of Turkey (YOK) fellowship to Y. Ferhatoglu and FMC Corp. grant.
- 5-Keto clomazone
- 5-OH clomazone
- DXP synthase
- MEP pathway
ASJC Scopus subject areas
- Agronomy and Crop Science
- Health, Toxicology and Mutagenesis