| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
2Interdepartmental Genetics Program, Clemson University, Clemson, South Carolina 29634-0375; and 3Horticulture Department, Poole Agriculture Center, Box 340375, Clemson University, Clemson, South Carolina 29634-0375
Received for publication March 27, 1998. Accepted for publication November 10, 1998.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
Key Words: 
-tubulin • dinitroaniline • Eleusine indica • goosegrass • herbicide resistance • microtubules • oryzalin • Poaceae
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
), was discovered in cotton and soybean production fields of South Carolina (Mudge, Gossett, and Murphy, 1984
) where trifluralin had been applied repeatedly for many years. Since then, there have been a number of reports documenting the occurrence of DNH-resistant goosegrass throughout the southeastern United States (Vaughn, 1986
; Vaughn and Vaughan, 1990
; Baird et al., 1992
).
Currently, three distinct biotypes of goosegrass are recognized. These biotypes are characterized based on their resistance to the anti-microtubule DNHs and are referred to as either susceptible (S), intermediately resistant (I), or highly resistant (R). Mudge and coworkers (Mudge, Gossett, and Murphy, 1984
) reported the I biotype to be 3.7-fold more resistant than the S biotype, and the R biotype to be 12-fold more resistant than the S biotype, based on reduction of plant dry mass. Similar results (i.e., I = 5.7-fold and R = 34-fold) were obtained using a root-growth bioassay, which determined the concentration of oryzalin that reduced radicle elongation by 50% (unpublished data). Based on mitotic index values, Vaughn and his colleagues characterized the I biotype as 50-fold more resistant, and the R biotype as 1000-fold more resistant, than the S biotype (Vaughn, Vaughan, and Gossett, 1990
).
In other weed species, DNH resistance is reported for green foxtail [Setaria viridis (L.) Beauv.] (Morrison, Todd, and Nawolsky, 1989
), Palmer amaranth (Amaranthus palmeri S. Wats) (Gossett, Murdock, and Toler, 1992
), Johnsongrass [Sorghum halepense (L.) Pers.] (Wills, Byrd, and Hurst, 1992
), rigid ryegrass (Lolium rigidum Gaudin) (McAlister, Holtum, and Powles, 1995
), and for foxtail millet [Setaria italica (L.) Beauv.] via hybridization with green foxtail (Wang et al., 1996
). DNH resistance was also induced experimentally by methylmethane sulfonate (EMS) treatment of Chlamydomonas reinhardtii Dang. (James et. al., 1988,
1993
). However, selection of DNH-resistant genotypes in EMS-mutagenized plants has not been successful, despite repeated attempts (Smeda and Vaughn, 1994
). Nonetheless, tubulin mutants have proven very useful for the analysis of microtubule structure, stability, and function in fungal, algal, and animal cells where they have been described (Cleveland and Sullivan, 1985
; Schibler and Cabral, 1986
; Jung and Oakley, 1990
; Lee and Huang, 1990
; Schibler and Huang, 1991
; Fujimura et al., 1992
; James et al., 1993
).
In a recent genetic analysis of the highly resistant R biotype, inheritance of anti-microtubule drug resistance was determined to be controlled by a single, recessive nuclear gene (Zeng and Baird, 1997
). In that study, nonparental phenotypes (i.e., intermediate levels of resistance between that of the S and R parents) were not observed in the F1 hybrids, nor in their F2 progenies. These results indicate that the phenotypically intermediate I biotype is not simply a hybrid of R and S biotypes. Rather, they suggest that the I phenotype is either controlled by a different locus than is the R and S phenotypes, or by a different allele at the same locus. The determination of the mode of inheritance of resistance in the I biotype will improve our understanding of the evolution and spread of resistance in plant populations and help elucidate the biochemical and molecular mechanisms of such resistance.
The objectives of this study were to characterize the inheritance and behavior of the I phenotype in comparison to the S and R phenotypes. These objectives were reached through making reciprocal crosses between the I biotype and the previously characterized R and S biotypes, identifying the F1 hybrids from each cross, determining the dinitroaniline-herbicide response phenotype (DRP) of the F1 plants and their F2 progenies, and analyzing segregation data with regard to the inheritance of DNH resistance in the I-biotype.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
; Zeng and Baird, 1997
; Yamamoto, Zeng, and Baird, 1998
).
Crosses and identification of F1 hybrids
Crosses were made between inbred lines of the I biotype and the R or S biotype. The crosses were made without emasculation, and the plants were pollinated by routine clipping and pollen transfer methods (Fehr, 1980
). All cross-pollinations were performed in the greenhouse.
The F1 hybrids were identified by screening the seeds produced by controlled crosses for two isozyme markers [isocitrate dehydrogenase (IDH) and acid phosphatase (ACP)]. The isozyme methodology and genetic description for these two isozyme markers in goosegrass followed standard procedures (Werth et al., 1993
; Werth, Hilu, and Langner, 1994
). Using IDH, individuals of the I biotype, FSC-I, were identified as homozygous for the Idh2b allele, and those of the S biotype, ASC-S, were homozygous for the Idh2a allele. Thus, F1 hybrids between I and S biotypes could be identified by their unique six-banded heterozygous phenotype. Using ACP, a dimeric enzyme, individuals of the I biotype, FSC-I, were classified as homozygous for the slow (s) allele; while those of the resistant biotype, MSC-R or CAL-R, were homozygous for the fast (f) allele. Thus, F1 hybrids between the I and R biotypes would display a three-banded, heterozygous pattern, with the middle band formed as a heterodimer of the f and s products. The identified F1 hybrids were transferred to growth chambers [14 h daylight (1 mmol photons·m-2·s-1) at 25° C; 10 h dark at 18° C] and selfed to produce F2 populations.
Dinitroaniline-herbicide response phenotypes of control and F1 plants
Because the DNHs act as preemergence herbicides killing seedlings with a susceptible phenotype, a bioassay was required that would determine the DRP of F1 plants, while allowing all individuals to survive and mature for advancement to the F2 generation. A rooting bioassay, which employs clonally propagated material, to screen mature plants for DNH resistance was modified for this purpose (Zeng and Baird, 1997
). Briefly, tillers were separated from the main crown and transferred to a solid culture medium amended with one of seven concentrations of oryzalin [designed from recommended field application rates for the active ingredient: 0.00 ppm, 0.04 ppm (1 x 10-7 mol/L), 0.17 ppm (5 x 10-7 mol/L), 0.28 ppm (8 x 10-7 mol/L), 0.69 ppm (2 x 10-6 mol/L), 3.46 ppm (1 x 10-5 mol/L), and 17.32 ppm (5 x 10-5 mol/L)]. Oryzalin (technical grade, 97% purity, Eli Lilly Company, Indianapolis, Indiana) was used for the experiments reported here because it is considered the model dinitroaniline (Strachan and Hess, 1983
). After 8 d of culture, the tillers were observed for their rooting response (i.e., adventitious root initiation, elongation, and morphology).
Three root-growth categories were easily delineated. Roots could be either inhibited (i.e., new roots were extremely short, thick, and brown in color with a dramatically swollen apex), marginally inhibited (i.e., new roots had elongated, but were relatively short and thick, with a swollen apex), or normal (i.e., new roots were very long, thin, and white in color with a naturally tapering apex). Depending upon the rooting response at different concentrations of oryzalin, control plants of the S, I, or R biotypes displayed the corresponding phenotype (i.e., S, I, or R phenotype, respectively).
The DRP of F1 plants was defined by comparison of the rooting response of their tillers to those from parental and control plants of known phenotype. At each concentration, the F1 plants of S x I were treated alongside their S and I parental plants, as well as the control R biotype plants. The possible DRP of the F1 plants of S x I could be either parental (i.e., S or I) or nonparental (i.e., more resistant than I; less resistant than I, but more than S; or more susceptible than S). Similarly, the F1 plants of I x R were treated alongside their I and R parental plants, as well as control S-biotype plants. Again, the possible DRP of the F1 plants of I x R could be either parental (i.e., I or R) or nonparental (i.e., more resistant than R; less resistant than I; or intermediate between R and I).
Differentiating the dinitroaniline-herbicide response phenotypes of control and F2 seedlings
The DRP of F2 seedlings and of seedlings from selfed parental plants with known S, I, and R phenotypes (control seedlings) was determined by a modified radicle elongation bioassay, as previously described (Beckie et al., 1990
; Zeng and Baird, 1997
). In this assay, the seeds were surface sterilized and plated in petri dishes (100 x 15 mm) on two layers of sterile cellulose filter paper (P5, Fisher Scientific, Pittsburgh, Pennsylvania) saturated with one of the seven concentrations of oryzalin. After germination, which was uniform and occurred within 12 h of planting, the seedlings were measured for their radicle length on day 8 postincubation.
The DRP of F2 seedlings was defined by comparing their radicle growth to that of control parental seedlings germinated alongside. Each plate contained selfed seeds from one F1 plant, 30–50 each, and seeds from the selfed S, I, and R control plants, 15 each. There were at least four replicates for each oryzalin concentration treatment. The observed segregation ratio between the S, I, R, or nonparental phenotypes in the F2 seedlings was tested for goodness of fit to various Mendelian inheritance patterns using Pearson chi-square test (Bliss, 1967
).
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
Dinitroaniline-herbicide response phenotypes of known biotypes
Rooting of tillers from parental plants was characterized. The rooting response of tillers from the S, I, and R biotypes was normal (i.e., not inhibited) when the culture medium was amended with oryzalin at 
0.04 ppm. The rooting of tillers from the S biotype was inhibited at 
0.17 ppm, while that of tillers from the R biotype was not inhibited until oryzalin was 17.32 ppm. The rooting response of tillers from the I biotype was intermediate between that of the S and R biotypes, i.e., normal at 0.17 ppm, marginally inhibited at 0.28 ppm and 0.69 ppm (Fig. 1A, B), and completely inhibited at 3.46 ppm (Table 1).
|
|
0.17 ppm. The radicle growth of control R biotype seedlings was not inhibited (i.e., at least 10 mm in length) until the oryzalin concentration was 3.46 ppm. Radicle growth of control I biotype seedlings was normal at 0.17 ppm, but was inhibited at 0.69 ppm. When treated at 0.28 ppm, radicle growth of control I biotype seedlings was distinctly intermediate between that of the S and R biotypes (Figs. 2A, B and 3). At this concentration, the lengths of radicles ranged from 11 to 26 mm for the R biotype, from 2 to 7 mm for the I biotype, and was completely inhibited for the S biotype. Therefore, S, I, and R biotypes could be distinguished simultaneously at a single concentration of 0.28 ppm oryzalin.
|
|
0.04 ppm, but was inhibited at 0.17 ppm. Nonparental phenotypes were not observed. Rooting of tillers from F1 plants of R x I was identical to that of their I parent (Fig. 1B, Table 1). Rooting of both F1 and their I parental plants was not inhibited in oryzalin at 0.17 ppm, was marginally inhibited at 0.28 and 0.69 ppm, and was completely inhibited at 3.46 ppm. Again, nonparental phenotypes were not observed.
Differentiating phenotypes of F2 seedlings
F2 seedlings of S x I were evaluated for their DRP at the discriminating concentration of 0.28 ppm oryzalin. Radicle length of F2 seedlings was either absent (i.e., 0 mm), similar to the S control seedlings, or ranged from 2 to 7 mm, similar to the I control seedlings. Thus, F2 seedlings without radicle elongation were classified as S phenotype, while those with radicle lengths between 2 and 7 mm were classified as I phenotype. Seedlings displaying nonparental phenotypes (e.g., >7 mm or between 0 and 2 mm) were not observed. Examples of the DRP of F2 seedlings treated at 0.28 ppm are shown in Fig. 2A. Figure 3 shows examples of bimodal distribution for the radicle length of F2 seedlings and continuous distribution for the control seedlings. The ratio of S seedlings to I seedlings in the F2 families of S x I best fit a 3:1 ratio by chi-square analysis (Table 2).
|
One hundred F2 seedlings for each of the eight F2 families were tested at other concentrations of oryzalin. F2 seedlings of S x I were all normal for their radicle growth at 0.04 ppm, showed 3:1 (i.e., inhibited : normal) segregation at 0.17 ppm, or all were inhibited in their radicle growth at 0.69 ppm. F2 seedlings of I x R were all normal for their radicle growth at 0.17 ppm, showed 3:1 (i.e., inhibited : normal) segregation at 0.69 ppm, or all were inhibited at 3.46 ppm oryzalin. Again, at all concentrations tested, nonparental phenotypes were not observed. Results are summarized in Table 3.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
). The susceptible phenotype of F1 plants of S x I indicated susceptibility to be dominant to intermediate resistance. Similarly, the intermediately resistant phenotype of F1 plants of R x I indicated intermediate resistance to be dominant to high resistance. Therefore, both forms of resistance to the antimicrotubule dinitroanilines in goosegrass are each recessive to susceptibility. In addition, there was no indication of an additive effect of resistance genes in F1 plants of R x I because the nonparental phenotype (i.e., more resistant to oryzalin than R parental plant) was not observed. Thus, these results suggest a simple genetic model for the explanation of DNH resistance in goosegrass (i.e., resistance in the I and R biotypes is inherited as a single nuclear gene trait). Results of DRP segregation analyses in F2 seedlings further supported and extended the conclusion obtained from analyses of F1 plants. The segregation ratios in F2 seedlings of S x I and R x I were consistently 3:1 (for S:I and I:R) across all eight F2 families tested at 0.28 ppm oryzalin. Thus, the DRP in the I biotype was inherited as a single nuclear gene. In addition, segregation analysis confirmed the dominance of the S phenotype over the I phenotype and the dominance of the I phenotype over the R phenotype.
Therefore, we conclude that the DRP in goosegrass is controlled by three alleles (i.e., Drp-S, Drp-i, and Drp-r for susceptibility, intermediate resistance, and high resistance, respectively) at a single Drp locus, such that Drp-S is dominant to Drp-i, and Drp-i is dominant to Drp-r. Based on this designation, the genotype of F1 plants of S x I is inferred to be Drp-S/Drp-i and that of F1 plants of R x I to be Drp-r/Drp-i. An allelic relationship among S, I, and R phenotypes is strongly suggested by our results. This simple genetic model for control of DNH resistance is also supported by analysis of F3 progenies (data not shown). The genotypes in F2 seedlings were inferred from the DRP of their F3 progenies. The ratio of inferred genotypes in F2 seedlings was 2:1 for Drp-S/Drp-i:Drp-S/Drp-S in rescued susceptible F2 plants of S x I and for Drp-i/Drp-r:Drp-i/Drp-i in rescued intermediate resistant F2 plants of I x R. This 2:1 ratio of inferred genotypes in F2 seedlings is most easily explained by the hypothesized simple genetic model.
Finally, the results do not unambiguously rule out the existence of two tightly linked genes contributing to the DRP. However, we believe that the large number (above 1000) of F2 seedlings tested here, as well as those reported in our previous studies (Baird et al., 1996b
; Zeng and Baird, 1997
), would have identified a rare recombinant (r > 0.001) if it had occurred.
As discussed in the previous study (Zeng and Baird, 1997
), the occurrence of the resistance allele (Drp-r) in high frequency in R populations could be explained by founder effect and natural selection imposed by repeated herbicide application. Similarly, the occurrence of the intermediate-resistance allele (Drp-i) in the I populations could also be explained by the same factors. In the population where the Drp-i allele was identified, the founder effect was promoted by self-fertilization, high fecundity, and lack of a specialized seed dispersal mechanism in goosegrass. In addition, application of the herbicide created a strong selection for the homozygous recessive phenotype. The relatively rare occurrence of the intermediate-resistance biotype (i.e., only known from a single location) compared with the more common occurrence of the highly resistant biotype could be explained by the different fitness of the two resistance phenotypes under field selection pressure. In fact, it is known that agricultural as well as wild populations of goosegrass are genetically quite distinct from one another (Baird et al., 1993
). Since the evolution of resistance alleles in plant populations is very likely from pre-existing genes (Maxwell and Mortimer, 1994
), the Drp-i or Drp-r alleles may coexist with Drp-S at very low frequency. The resistance allele will be selected upon herbicide application. Thus, a population with high frequency of Drp-i or Drp-r will evolve. When all three alleles exist in a single population, it is likely that selection may favor the Drp-r allele. This may explain the predominance of R populations identified from agriculture sites (Mudge, Gossett, and Murphy, 1984
; Baird et al., 1992
).
The DNHs decrease the stability of spindle and cortical microtubules, essential determinants of plant growth and development (Lloyd, 1987
), by interfering with tubulin dimer polymerization (Morejohn et al., 1987
). This phenomenon has been demonstrated both in vivo (Cleary and Hardham, 1988
) and in vitro (Strachan and Hess, 1983
; Morejohn et al., 1987
). Destabilization and inhibition of microtubule assembly are suggested to result from the direct binding of DNHs to tubulin dimers. This binding then interferes with polymerization of tubulins into microtubules and thus, microtubule stability (Strachan and Hess, 1983
; Morejohn et al., 1987
; Hugdahl and Morejohn, 1993
).
The most plausible explanation for the DNH resistance in the resistant biotypes is an alteration of the cellular target site of the DNHs (i.e., the tubulin subunits of microtubules) (Chernicky, 1985
). It is well established from work with Chlamydomonas that tubulin mutations conferring resistance to anti-microtubule herbicides can result from amino acid substitutions that alter the electrophoretic mobility of or ß tubulins (Bolduc, Lee, and Huang, 1988
; Lee and Huang, 1990
; Schibler and Huang, 1991
; James et al., 1993
). In goosegrass, a new ß tubulin polypeptide was observed in an R biotype (Vaughn and Vaughan, 1990
). One published study concluded there was no evidence that resistance to dinitroaniline herbicides is associated with a modified tubulin polypeptide (Waldin, Ellis and Hussey, 1992
), while another report from the same group implicated an tubulin in the resistance phenomenon (Waldin and Hussey, 1993
). Southern blot analysis of tubulin gene families in the three goosegrass biotypes indicated that the mutation is most likely to be a point mutation, rather than the result of a larger deletion(s) or insertion(s) (Mysore and Baird, 1995
). The allelic relationship between the I and R phenotypes implies that DNH resistance in I and R biotypes is controlled by similar biochemical/molecular mechanisms. Therefore, the allelic relationship between the I and R phenotypes is consistent with the hypothesis that a tubulin mutation(s) confers DNH resistance in goosegrass. Recent studies have identified a point mutation in an -tubulin from the R biotype (Cronin et al., 1993
; Yamamoto, Zeng, and Baird, 1998
) and another from the I biotype (Yamamoto, Zeng, and Baird, 1998
) that correlate with DNH resistance and with an tubulin of altered electrophoretic mobility from the R biotype (Baird et al., 1996a
). Although less likely now (Anthony et al., 1998
), mutations in other nontubulin genes (e.g., MAPs or posttranslational modification pathways) cannot be completely ruled out as contributing to the resistant phenotype(s), especially when considering the number, and widespread distribution, of DNH resistant goosegrass populations.
This study is the first to characterize inheritance of DNH resistance in a species displaying multiple resistance levels. The information provided in this study will help to further our understanding of the genetic and biochemical mechanisms of anti-microtubule drug resistance, as well as the evolution and spread of DNH resistance in plant populations. Considering the agronomic importance of goosegrass, the high level of anti-microtubule drug resistance, and the existence of a second less tolerant biotype, the determination of inheritance of DNH resistance in our studies makes goosegrass a powerful model system in which to study the cellular and molecular mechanisms of resistance.
|
FOOTNOTES |
|---|
4 Current address: U.S. Salinity Laboratory, USDA/ARS, 450 W. Big Springs Rd., Riverside, CA 92507.
5 Author for correspondence: vbaird@Clemson.edu.
|
LITERATURE CITED |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
Baird, W. V., C. A. Langner, J. Wells, K. Tucker, T. Whitwell, and C. R. Werth. 1992 Dinitroaniline resistant goosegrass [Eleusine indica (L.) Gaertn.] from the southeastern United States: characterization of biotypes and population genetic analysis. American Journal of Botany 79: 89–90 (Abstract).
———, L. Morejohn, L. Zeng, K. Mysore, and H-H. Kim. 1996a Genetic, molecular and biochemical characterization of dinitroaniline herbicide resistance in goosegrass (Eleusine indica). Second International Weed Control Congress. Copenhagen, Denmark.
———, C. R. Werth, J. Wells, L. Zeng, and K. Mysore. 1993 Genetic divergence and identity in populations of goosegrass (Eleusine indica) displaying different herbicide response phenotypes. Second South Carolina Statewide Research Conference. Isle of Palms, SC, U.S.A. (abstract number D13); Clemson University Publishing, Clemson, SC.
———, L. Zeng, K. Koka, and E. Yamamoto. 1996b Genetic and molecular analysis of dinitroaniline resistance in three biotypes of goosegrass (Eleusine indica). Xe Colloque International Sur la Biologie des Mauvaises Herbes, 181–188. Dijon, France.
Beckie, H. J., L. F. Friesen, K. M. Nawolsky, and I. N. Morrison. 1990 A rapid bioassay to detect trifluralin-resistant green foxtail (Setaria viridis). Weed Technology 4: 505–508.[ISI]
Bliss, C. I. [ed.]. 1967 Statistics in biology. McGraw-Hill, New York, NY.
Bolduc, S., V. D. Lee, and B. Huang. 1988 Beta-tubulin mutants of the unicellular green alga Chlamydomonas reinhardtii. Proceedings of the National Academy of Sciences, USA. 85: 131–135.
Chernicky, J. P. 1985. An investigation into the resistance of goosegrass (Eleusine indica) to dinitroaniline herbicides. Ph.D. dissertation, University of Illinois at Urbana-Champaign, Urbana, IL.
Cleary, A. L., and A. R. Hardham. 1988 Depolymerization of microtubule arrays in root tip cells by oryzalin and their recovery with modified nucleation patterns. Canadian Journal of Botany 66: 2353–2366.
Cleveland, D. W., and K. F. Sullivan. 1985 Molecular biology and genetics of tubulin. Annual Review of Biochemistry 54: 331–365.[CrossRef][ISI][Medline]
Cronin, K., P. Hussey, J. Ray, and T. Waldin. 1993 Herbicide resistant plants. World Intellectual Property Organization International Publication Number. 93/24637.
Fehr, W. R. 1980 Artificial hybridization and self-pollination. In W. R. Fehr and H. H. Hadley [eds.], Hybridization of crop plants, 105–131. American Society of Agronomy and Crop Science Society of America, Madison, WI.
Fujimura, M., T. Kamakura, H. Inoue, S. Inoue, and I. Yamaguchi. 1992 Sensitivity of Neurospora crassa to benzimidazoles and N-phenylcarbamates—Effect of amino acid substitutions at position 198 in ß-tubulin. Pesticide Biochemistry and Physiology 44: 165–173.[CrossRef][ISI]
Gossett, B. J., E. C. Murdock, and J. E. Toler. 1992 Resistance of Palmer amaranth (Amaranthus palmeri) to the dinitroaniline herbicides. Weed Technology 6: 587–591.[ISI]
Holm, L. G., D. L. Plucknett, J. V. Pancho and J. P. Herberger. 1991 The world's worst weeds. Kriegen Publishing Co., Malabar, FL.
Hugdahl, J. D., and L. C. Morejohn. 1993 Rapid and reversible high-affinity binding of the dinitroaniline herbicide oryzalin to tubulin from Zea mays L. Plant Physiology 102: 725–740.
James, S . W., L. P. W. Ranum, C. D. Silflow, and P. A. Lefebvre. 1988 Mutants resistant to anti-microtubule herbicides map to a locus on the uni linkage group in Chlamydomonas reinhardtii. Genetics 118: 141–147.
———, C. D. Silflow, P. Stroom, and P. A. Lefebvre. 1993 A mutation in the 1-tubulin gene of Chlamydomonas reinhardtii confers resistance to anti-microtubule herbicides. Journal of Cell Science 106: 209–218.[Abstract]
Jung, M. K., and B. R. Oakley. 1990 Identification of an amino acid substitution in the benA, ß-tubulin gene of Aspergillus nidulans that confers thiabendazole resistance and benomyl supersensitivity. Cell Motility and the Cytoskeleton 17: 87–94.[CrossRef][ISI][Medline]
Lee, V. D., and B. Huang. 1990 Missense mutations at lysine 350 in ß-tubulin confer altered sensitivity to microtubule inhibitors in Chlamydomonas. Plant Cell 2: 1051–1057.
Lloyd, C. W. 1987 The plant cytoskeleton: the impact of fluorescence microscopy. Annual Review of Plant Physiology 38: 119–139.[CrossRef][ISI]
Maxwell, B. D., and A. M. Mortimer. 1994 Selection for herbicide resistance. In S. B. Powles and J. A. M. Holtum [eds.], Herbicide resistance in plants: biology and biochemistry, 1–25. Lewis Publishers, Boca Raton, FL.
McAlister, F. M., J. A. M. Holtum and S. B. Powles. 1995 Dinitroaniline herbicide resistance in rigid ryegrass (Lolium rigidum). Weed Science 43: 55–62.
Morejohn, L. C., T. E. Bureau, J. Mole-Bajer, A. S. Bajer, and D. E. Fosket. 1987 Oryzalin, a dinitroaniline herbicide, binds to plant tubulin and inhibits microtubule polymerization in vitro. Planta 172: 252–264.
Morrison, I. N., B. G. Todd, and K. M. Nawolsky. 1989 Confirmation of trifluoralin-resistant green foxtail (Setaria viridis) in Manitoba. Weed Technology 3: 544–551.[ISI]
Mudge, L. C., B. J. Gossett, and T. R. Murphy. 1984 Resistance of goosegrass (Eleusine indica) to dinitroaniline herbicides. Weed Science 32: 591–594.[ISI]
Mysore, K., and V. Baird. 1995 Molecular characterization of the tubulin-related gene families in herbicide resistant and susceptible goosegrass (Eleusine indica). Weed Science 43: 28–33.[ISI]
Schibler, M. J., and F. Cabral. 1986 Taxol-dependent mutants of Chinese hamster ovary cells with alterations in - and ß-tubulin. Journal of Cell Biology 102: 1522–1531.
———, and B. Huang. 1991 The colR4 and colR15 beta-tubulin mutations in Chlamydomonas confer altered sensitivities to microtubule inhibitors and herbicides by enhancing microtubule stability. Journal of Cell Biology 113: 605–614.
Smeda, R. J., and K. C. Vaughn. 1994 Resistance to dinitroaniline herbicides. In S. B. Powels and J. A. M. Holtum [eds.], Herbicide resistance in plants: biology and biochemistry, 215–228. CRC Press, Boca Raton, FL.
Strachan, S. D., and F. D. Hess. 1983 The biochemical mechanism of action of the dinitroaniline herbicide oryzalin. Pesticide Biochemistry and Physiology 20: 141–150.[CrossRef][ISI]
Vaughn, K. C. 1986 Cytological studies of dinitroaniline-resistant Eleusine. Pesticide Biochemistry and Physiology 26: 66–74.
———, and M. A. Vaughan. 1990 Structural and biochemical characterization of dinitroaniline-resistant Eleusine. In H. M. LeBaron and W. K. Moberg [eds.], Managing resistance to agrochemicals: from fundamental research to practical strategies, 364–375. American Society of Chemistry, Los Angeles, CA.
———, ———, and B. J. Gossett. 1990 A biotype of goosegrass (Eleusine indica) with an intermediate level of dinitroaniline resistance. Weed Technology 4: 157–162.[ISI]
Waldin, T. R., J. R. Ellis and P. Hussey. 1992 Tubulin-isotype analysis of two grass species-resistant to dinitroaniline herbicides. Planta 188: 258–264.[CrossRef][ISI]
———, and P. J. Hussey. 1993 Expression of an altered tubulin isotype in a dinitroaniline herbicide resistant grass. Journal of Experimental Botany 44 (Supplement): 993.
Wang, T., A. Fleury, J. Ma, and H. Darmency. 1996 Genetic control of dinitroaniline resistance in foxtail millet (Setaria italica). Journal of Heredity 87: 423–426.
Werth, C. R., K. W. Hilu, and C. A. Langner. 1994 Isozymes of Eleusine (Gramineae) and the origin of finger millet. American Journal of Botany 81: 1186–1197.[CrossRef][ISI]
———, ———, ———, and W. V. Baird. 1993 Duplicate gene expression for isocitrate dehydrogenase and phosphoglutonate dehydrogenase in diploid species of Eleusine (Gramineae). American Journal of Botany 80: 705–710.[CrossRef][ISI]
Wills, G. D., J. D. Byrd, and H. R. Hurst. 1992 Herbicide resistant and tolerant weeds. Proceedings of Southern Weed Science Society 45: 43.
Yamamoto, E., L. Zeng, and W. V. Baird. 1998 Alpha-tubulin missense mutations correlate with anti-microtubule drug resistance in Eleusine indica. Plant Cell 10: 297–308.
Zeng, L., and W. V. Baird. 1997 Genetic basis of dinitroaniline herbicide resistance in a highly resistant biotype of goosegrass (Eleusine indica). Journal of Heredity 88: 427–432.
This article has been cited by other articles:
|
|
 |
|
  J. Feng Microtubule: A Common Target for Parkin and Parkinson's Disease Toxins Neuroscientist, December 1, 2006; 12(6): 469 - 476. [Abstract] [PDF]
|
|
|
|
 |
|
 C. Delye, Y. Menchari, S. Michel, and H. Darmency Molecular Bases for Sensitivity to Tubulin-Binding Herbicides in Green Foxtail Plant Physiology, December 1, 2004; 136(4): 3920 - 3932. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. S. Morrissette, A. Mitra, D. Sept, and L. D. Sibley Dinitroanilines Bind {alpha}-Tubulin to Disrupt Microtubules Mol. Biol. Cell, April 1, 2004; 15(4): 1960 - 1968. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W.-L. Wu, B. A. Schaal, C.-Y. Hwang, M.-D. Hwang, Y.-C. Chiang, and T.-Y. Chiang Characterization and adaptive evolution of {alpha}-tubulin genes in the Miscanthus sinensis complex (Poaceae) Am. J. Botany, October 1, 2003; 90(10): 1513 - 1521. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
