TY - JOUR
T1 - Fenoxaprop-P resistance in Phalaris minor conferred by an insensitive acetyl-coenzyme A carboxylase
AU - Tal, Abraham
AU - Zarka, Shalom
AU - Rubin, Baruch
PY - 1996/10
Y1 - 1996/10
N2 - A Phalaris minor population putatively resistant to fenoxaprop-P was identified in a wheat field in Israel during 1993. Dose-response studies conducted under controlled conditions with this biotype indicated a 20-fold increase in resistance to fenoxaprop-P compared with a susceptible biotype. The resistant biotype had also slight enhanced resistance (1,1 - to 3.0-fold) to acetyl-coenzyme A carboxylase (ACCase) inhibitors such diclofop, clodinafop, sethoxydim, and tralkoxydim, but was equally susceptible to propanil, isoproturon, and methabenzthiazuron, which do not inhibit this enzyme. Absorption, translocation, and metabolism were similar in both resistant and susceptible biotypes based on studies with [14C]fenoxaprop-P, indicating that resistance is due to another mechanism. ACCase from the resistant biotype was 19-fold less sensitive to fenoxaprop-P than that from the susceptible biotype, and 1.5- to 5-fold less sensitive to clodinafop, tralkoxydim, and cycloxydim. The close association between dose response at the whole-plant level and ACCase sensitivity to fenoxaprop-P and other ACCase-inhibiting herbicides suggests that resistance of P. minor to fenoxaprop-P is conferred by a modified ACCase.
AB - A Phalaris minor population putatively resistant to fenoxaprop-P was identified in a wheat field in Israel during 1993. Dose-response studies conducted under controlled conditions with this biotype indicated a 20-fold increase in resistance to fenoxaprop-P compared with a susceptible biotype. The resistant biotype had also slight enhanced resistance (1,1 - to 3.0-fold) to acetyl-coenzyme A carboxylase (ACCase) inhibitors such diclofop, clodinafop, sethoxydim, and tralkoxydim, but was equally susceptible to propanil, isoproturon, and methabenzthiazuron, which do not inhibit this enzyme. Absorption, translocation, and metabolism were similar in both resistant and susceptible biotypes based on studies with [14C]fenoxaprop-P, indicating that resistance is due to another mechanism. ACCase from the resistant biotype was 19-fold less sensitive to fenoxaprop-P than that from the susceptible biotype, and 1.5- to 5-fold less sensitive to clodinafop, tralkoxydim, and cycloxydim. The close association between dose response at the whole-plant level and ACCase sensitivity to fenoxaprop-P and other ACCase-inhibiting herbicides suggests that resistance of P. minor to fenoxaprop-P is conferred by a modified ACCase.
UR - http://www.scopus.com/inward/record.url?scp=0030265307&partnerID=8YFLogxK
U2 - 10.1006/pest.1996.0067
DO - 10.1006/pest.1996.0067
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AN - SCOPUS:0030265307
SN - 0048-3575
VL - 56
SP - 134
EP - 140
JO - Pesticide Biochemistry and Physiology
JF - Pesticide Biochemistry and Physiology
IS - 2
ER -