Atrazine resistance, mutation

In contrast, Ernst et al, (1996) have shown that a substitution at Ser264 does not necessarily lead to herbicide resistance. They found both Ser and Gly at position 264 in various sensitive and resistant biotypes of common groundsel. However, all resistant biotypes of black nightshade had Gly at position 264, but some of the sensitive biotypes also had Gly at this position. They suggested that the effect of this mutation in sensitive biotypes was overcome by two additional mutations in these biotypes alanine at position 251 (Ala25i) to arginine (Arg) and valine at position 280 (Val280) to leucine (Leu). In sensitive common lambsquarters, only Ser was present at position 264 either Ser or Gly were detected at position 264 in different atrazine-resistant plants (Ernst et al, 1996). 

Alfonso, M., J.J. Pueyo, K. Gaddour, A.-L. Etienne, D. Kirilovsky, and R. Picorel (1996). Induced new mutation of D1 serine-268 in soybean photosynthetic cell cultures produced atrazine resistance, increased stability of S2QB- and S3QB- states, and increased sensitivity to light stress. Plant Physiol., 112 1499-1508. 

Smeda et al. (1993) reported that in a mutation of the psb A gene in a photoautotropic potato, atrazine resistance was attributable to a mutation from AGT (ser) to ACT (threonine) in codon 264 of the psb A gene that encodes the Qb protein. Although the mutant cells exhibited extreme levels of resistance to atrazine, no concomitant reductions in photosynthetic electron transport or cell growth rates were detected compared to the unselected cells. This is in contrast with the losses in productivity observed in atrazine-resistant mutants that contain a Ser to Gly 264 alteration. Research has shown that triazine resistance by various algae and photosynthetic bacteria has been due to changes in many different binding sites (Oettmeier, 1999). 

Bettini, P, S. McNally, M. Sevignac, H. Darmency, J. Gasquez, and M. Dron (1987). Atrazine resistance in Chenopodium album Low and high levels of resistance to the herbicide are related to the same chloroplast psb A gene mutation. Plant Physiol., 84 1442-1446. Beversdorf, W.D., B.J. Hume, and M.J. Donelly-Vanderloo (1988). Agronomic performance of triazine-resistant and susceptible reciprocal spring canola hybrids. Crop Sci., 22 932-934. 

Gasquez, J. (1991). Mutation and atrazine resistance in Chenopodium album. In J.C. Caseley, G.W. Cussans, and R.K. Atkin, eds., Herbicide Resistance in Weeds and Crops. Oxford, UK Butterworth-Heinemann Ltd, pp. 103-113. 

In addition, we observed that Type I mutants have all of their psbA gene copies mutated (99.9% probability) while no heteroplasmicity was found in Sp. plants (19). This indicates that a mechanism other than a high mutation rate must work to allow the release of individual plants that have their entire chloroplast population mutated. This could be due to the control of chloroplast DNA replication directed by mitochondrial or nuclear genomes. Indeed, a sequence homology has been found between mitochondrial DNA and part of the chloroplast psbA gene. Moreover, this homologous sequence is expressed as an RNA transcript in atrazine resistant C. album only and not in the susceptible plants (30). 

As already stressed, the mutation Set264 Gly is one which has been observed in nature. It is found by now in all countries and in a variety of weeds which are rendered resistant t ainst triazines and triazinones (see Table 1). It should be noted, that atrazine-resistant rape with a modified Dl protein (Ser264 Gly) is used as a crop in Canada. Resistance against ureas is comparably small and against phenolic herbicides like i-dinoseb, ioxynil and DNOC negative cross resistance is observed. 

Masabni et al (1996) identified a Ser264 to Thr (threonine) mutation in a resistant biotype of common purslane. This conferred a high level of resistance to atrazine and also to linuron, a substituted urea herbicide. This was the first report of a Ser264 to Thr substitution in higher plants selected under field conditions. Previously, this mutation had only been selected through tissue culture in tobacco and potato (Sigematsu et al, 1989 Smeda etal, 1993). 

Of the 869 families derived from plants collected in five populations (Table II), 33 showed at least one seedling with an intermediary fluorescence curve (Figure 1 (21)). These seedlings proved later to have the mutated psbA gene at Position 264 (19) and were moderately resistant to atrazine. They were called Type I (for intermediate level of resistance). The 33 mother plants and their corresponding seed families were called Sp. because they were special susceptible plants that produced mutant plants. 

In 1999 Masabni and Zandstra reported on a mutant of Portulaca oleracea with a resistance pattern to PS II inhibitors that was different to most triazine resistant weeds [28], This mutant was resistant to the phenylureas linuron and diuron, but also cross-resistant to atrazine and other triazines. Sequencing of the D1 protein revealed that in the resistant biotype the serine 264 was replaced by threonine and not by glycine. This was the first report on a serine 264 to threonine mutation on a whole plant level. It was proposed that the serine-to-threonine mutation modified the conformation of the herbicide binding niche at the D1 protein in a way, which resulted in reduced binding of phenylureas and triazines as well. 

In order to determine the mutations present in DCMU-II, DCMU-IIg, AzI, AzV, loxi, we have cloned and sequenced the mutated pshk gene of the five mutants as well as the corresponding wild type (4,5,6). Table 1 shows the aminoacid changes in Dj for the five mutants as compared to the wild type. DCMU-II and AzV were obtained from DCMU-IIa and AzI after a second selection. As expected they both have a double mutation in the Dj sequence. In Chenopodiim album it is the substitution of Ser254 by Glycine which leads to the resistance to Atrazine. 

TABLE 1, Resistance against atrazine and compar.compounds Mutations in psbA causing amino acid substitutions in protein D1 ( Qg) of photosystem II... 

All but one of the 50 weed species that evolved resistance to atrazine or simazine in maize, in orchards or along roadsides, have a chloroplast genome mutation in the... 

There are a number of factors which can contribute to herbicide selectivity, including soil placement, rates of absorption and subsequent translocation, localization (both within the plant and at the subcellular level), and transformation to products of modified phytotoxicity. In addition, the recent work on the elucidation of the modes of action of the aryloxyphenoxypropionate and cyclohexanedione groups of herbicides has highlighted the importance of species differences in sensitivity of the target site, in this case the enzyme acetyl-CoA carboxylase. The monocot and dicot enzymes studied to date show a remarkable difference in sensitivity to these herbicides which correlates very well with the high level of resistance among dicots. Biotypes of Chenopodium album and Amaranthus hybridus L. resistant to atrazine as a result of a mutation in the 32-kDa protein component of photosystem II would constitute a further example. 

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