Avena fatua L., wild oat (Poaceae).

Author(s):  
S. M. Boyetchko
Keyword(s):  
Weed Science ◽  
1974 ◽  
Vol 22 (5) ◽  
pp. 476-480 ◽  
Author(s):  
Robert W. Neidermyer ◽  
John D. Nalewaja

The response of wheat (Triticum aestivum L.) and wild oat (Avena fatua L.) to barban (4-chloro-2-butynyl-m-chlorocarbanilate) was studied as influenced by plant morphology and air temperature after application. Growth of wheat and wild oat seedlings was reduced by barban at 0.3 μg and 0.6 μg applied to the first node, respectively. Barban application to the base and midpoint of the first leaf blade required a lower dose to reduce wild oat growth than wheat growth. Increased tillering occurred from barban injury to the main culm in wheat. Wheat and wild oat susceptibility to barban increased as the post-treatment temperature decreased from 32 to 10 C. Barban selectivity for wild oats in wheat was greater at 27 and 21 C than at 16 and 10 C.


Weed Science ◽  
1983 ◽  
Vol 31 (5) ◽  
pp. 693-699 ◽  
Author(s):  
Blaik P. Halling ◽  
Richard Behrens

Experiments were conducted with isolated protoplasts of wild oat (Avena fatuaL. # AVEFA) and isolated chloroplasts of wild oat and wheat (Triticum aestivumL.), to determine if the methyl sulfate salt of difenzoquat (1,2-dimethyl-3,5-diphenyl-1H-pyrazolium) might influence photoreactions in these species. Difenzoquat did not affect CO2fixation, uncoupled electron transport, or proton uptake. At concentrations of 0.5 mM and 1 mM, difenzoquat caused a slight, but statistically significant, inhibition of photophosphorylation. Experiments assaying coupled electron transport indicated that inhibition of photophosphorylation occurred not through uncoupling, but by an energy-transfer inhibition. This same effect was observed in isolated mitocondria of both species, with about 50% inhibition of state 3 respiration rates occurring with 10 μM difenzoquat. However, no important differentials were observed in the relative susceptibilities of wheat and wild oat mitochondria. Difenzoquat also functioned as a weak autooxidizing electron acceptor in photosynthetic electron transport. Therefore, difenzoquat-induced leaf chlorosis and necrosis may result from a bipyridilium-type electron acceptor activity if sufficient herbicide is absorbed.


2010 ◽  
Vol 50 (1) ◽  
pp. 41-44 ◽  
Author(s):  
Khawar Jabran ◽  
Muhammad Farooq ◽  
Mubshir Hussain ◽  
Muhammad Ali ◽  

Wild Oat (Avena FatuaL.) and Canary Grass (Phalaris MinorRitz.) Management Through AllelopathyEnvironmental contamination, herbicide resistance development among weeds and health concerns due to over and misuse of synthetic herbicides has led the researchers to focus on alternative weed management strategies. Allelochemicals extracted from various plant species can act as natural weed inhibitors. In this study, allelopathic extracts from four plant species sorghum [Sorghum bicolor(L.) Moench], mulberry (Morus albaL.), barnyard grass [Echinochloa crusgalli(L.) Beauv.], winter cherry [Withania somnifera(L.)] were tested for their potential to inhibit the most problematic wheat (Triticum aestivumL.) weeds wild oat (Avena fatuaL.) and canary grass (Phalaris minorRitz.). Data regarding time to start germination, time to 50% germination, mean germination time, final germination percentage, germination energy, root and shoot length, number of roots, number of leaves, and seedling fresh and dry weight was recorded for both the weeds, which showed that mulberry was the most inhibitory plant species while sorghum showed least allelopathic suppression against wild oat. Mulberry extracts resulted in a complete inhibition of the wild oat germination. The allelopathic potential for different plants against wild oat was in the order: mulberry > winter cherry > barnyard grass > sorghum. Mulberry, barnyard grass and winter cherry extracts resulted in a complete inhibition of canary grass. Sorghum however exhibited least suppressive or in some cases stimulatory effects on canary grass. Plants revealing strong allelopathic potential can be utilized to derive natural herbicides for weed control.


2012 ◽  
Vol 92 (5) ◽  
pp. 923-931 ◽  
Author(s):  
H. J. Beckie ◽  
S. Shirriff

Beckie, H. J. and Shirriff, S. 2012. Site-specific wild oat ( Avena fatua L.) management. Can. J. Plant Sci. 92: 923–931. Variation in soil properties, such as soil moisture, across a hummocky landscape may influence wild oat emergence and growth. To evaluate wild oat emergence, growth, and management according to landscape position, a study was conducted from 2006 to 2010 in a hummocky field in the semiarid Moist Mixed Grassland ecoregion of Saskatchewan. The hypothesis tested was that wild oat emergence and growth would be greater in lower than upper slope positions under normal or dry early growing season conditions. Three herbicide treatments were imposed on the same plots each year of a 2-yr canola (Brassica napus L.) – wheat (Triticum aestivum L.) sequence: (1) nontreated (weedy) control; (2) herbicide application to upper and lower slope positions (i.e., full or blanket application); and (3) herbicide application to lower slope position only. Slope position affected crop and weed densities before in-crop herbicide application in years with dry spring growing conditions. Site-specific wild oat herbicide application in hummocky fields in semiarid regions may be justified based on results of wild oat control averaged across slope position. In year 2 of the crop sequence (wheat), overall (i.e., lower and upper slope) wild oat control based on density, biomass, and dockage (i.e., seed return) was similar between site-specific and full herbicide treatment in 2 of 3 yr. Because economic thresholds have not been widely adopted by growers in managing wild oat, site-specific treatment in years when conditions warrant may be an appropriate compromise between no application and blanket herbicide application.


1979 ◽  
Vol 59 (1) ◽  
pp. 93-98 ◽  
Author(s):  
F. A. QURESHI ◽  
W. H. VANDEN BORN

Uptake of 14C-diclofop-methyl {methyl 2-[4-(2,4-dichlorophenoxy)phenoxy propanoate]} by leaves of wild oats (Avena fatua L.) was reduced significantly in the presence of MCPA {[(4-chloro-o-tolyl)oxy]acetic acid]}, especially the dimethylamine formulation. If the herbicides were applied separately, the degree of interference with uptake depended on the extent of overlap of droplets of the two spray preparations on the leaf surface. Spray volume and direction of spray application were important factors in minimizing the mixing of spray droplets on the leaves if the two herbicides were applied separately with a tandem arrangement of two sprayers. Such a sequential application of MCPA ester and diclofop-methyl in a field experiment provided significantly greater wild oat control than could be obtained with a tank mix of the same two herbicides, but the results were not consistent enough to recommend the procedure for practical use.


Weed Science ◽  
1980 ◽  
Vol 28 (6) ◽  
pp. 725-729 ◽  
Author(s):  
B. D. Hill ◽  
B. G. Todd ◽  
E. H. Stobbe

The basis for 2,4-D [(2,4-dichlorophenoxy)acetic acid] antagonism of diclofop-methyl {methyl 2-[4-(2,4-dichlorophenoxy) phenoxy] propanoate} toxicity to wild oat (Avena fatuaL.) was investigated by studying changes in the metabolism of diclofop-methyl in vitro. An esterase from wild oat, which hydrolyzes diclofop-methyl to the acid diclofop, was extracted, partially purified, and the reaction characterized. The rate of hydrolysis of14C-diclofop-methyl was 0.14 ηmoles/2 h at standard assay conditions of 0.25 mg lyophilized enzyme preparation (19.6% protein) in 0.1 ml phosphate buffer (0.1 M, pH 7.0), substrate 5 μM. The addition of 2,4-D to this reaction did not inhibit14C-diclofop formation. Higher levels of 2,4-D stimulated enzymic hydrolysis.14C-diclofop-methyl was rapidly metabolized to14C-diclofop and polar14C-conjugates when vacuum-infiltrated into wild oat leaf segments. The addition of 2,4-D caused small increases in the rates of both14C-diclofop-methyl de-esterification and14C-diclofop conjugation. It is concluded that 2,4-D does not inhibit the in vitro de-esterification of diclofop-methyl.


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