scholarly journals Structure of the CAC1 Gene and in Situ Characterization of Its Expression (The Arabidopsis thaliana Gene Coding for the Biotin-Containing Subunit of the Plastidic Acetyl-Coenzyme A Carboxylase)

1997 ◽  
Vol 113 (2) ◽  
pp. 357-365 ◽  
Author(s):  
J. Ke ◽  
J. K. Choi ◽  
M. Smith ◽  
H. T. Horner ◽  
B. J. Nikolau ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Coenzyme A ◽  
In Situ Characterization ◽  
Acetyl Coenzyme A ◽  
Acetyl Coenzyme ◽  
Gene Coding ◽  
Acetyl Coenzyme A Carboxylase

Characterization of Fenoxaprop-P-Ethyl–Resistant Junglerice (Echinochloa colona) from Mississippi

Weed Science ◽  
2016 ◽  
Vol 64 (4) ◽  
pp. 588-595 ◽  
Author(s):  
Alice A. Wright ◽  
Vijay K. Nandula ◽  
Logan Grier ◽  
Kurt C. Showmaker ◽  
Jason A. Bond ◽  
...  
Keyword(s):  
Coenzyme A ◽  
Point Mutations ◽  
Target Site ◽  
Acetyl Coenzyme A ◽  
Acetyl Coenzyme ◽  
Resistant Population ◽  
Sunflower County ◽  
Acetyl Coenzyme A Carboxylase ◽  
P450 Inhibitors

A population of junglerice from Sunflower County, MS, exhibited resistance to fenoxaprop-P-ethyl. An 11-fold difference in ED50 (the effective dose needed to reduce growth by 50%) values was observed when comparing the resistant population (249 g ae ha–1) with susceptible plants (20 g ae ha–1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim at the field rate. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P-ethyl, did not reveal the presence of any known resistance-conferring point mutations. An enzyme assay confirmed that the acetyl coenzyme A carboxylase in the resistant population is herbicide sensitive. Further investigations with two cytochrome P450 inhibitors, malathion and piperonyl butoxide, and a glutathione-S-transferase inhibitor, 4-chloro-7-nitrobenzofurazan, did not indicate involvement of any metabolic enzymes inhibited by these compounds. The absence of a known target-site point mutation and the sensitivity of the ACCase enzyme to herbicide show that fenoxaprop-P-ethyl resistance in this population is due to a non–target-site mechanism or mechanisms.

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