Published in Crop Sci. 44:125-130 (2004).
© 2004 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA
CROP BREEDING, GENETICS & CYTOLOGY
Comparison of Different Sources of Vector Resistance for Controlling Wheat Streak Mosaic in Winter Wheat
J. B. Thomas*,a,
R. L. Connerb and
R. J. Grafc
a Cereal Research Centre, Agriculture and Agri-Food Canada, 195 Dafoe Road, Winnipeg, MB, R3T 2M9, Canada
b Morden Research Station, Agriculture and Agri-Food Canada, Unit 100-101, Route 100, Morden, MB, R6M 1Y5, Canada
c Lethbridge Research Centre, Agriculture and Agri-Food Canada, P.O. Box 3000, Lethbridge, AB, T1J 4B1, Canada
* Corresponding author (jthomas{at}em.agr.ca).
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ABSTRACT
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Wheat streak mosaic (WSM) is a serious viral disease of wheat (Triticum aestivum L.) that is vectored by the wheat curl mite (Aceria tosichella Keifer). Deployment of wheat cultivars with vector resistance is a possible method for WSM control. This 3-yr (1996–1997/1998–1999) field study compared by means of a split-plot design the effect of different sources of mite-resistance backcrossed into a common winter wheat genetic background on both the spread of WSM and on the resulting yield losses. The various lines were first seeded early (in July) in blocks of spaced plots to provide different disease source or spreader treatments as main plots. The same winter wheat lines were then seeded in mid-September into the spaces between the spreaders as subplot treatments to mimic the crop. Main-plot (spreader) treatments included the mite-susceptible winter wheat cultivars CDC Kestrel or Norstar, two mite-resistant backcross lines of Norstar with resistance from Thinopyrum ponticum (Podpera) Liu & Wang (Nst*5/Cmc2) and Triticum tauschii (Coss.) Schmal. (Nst*5/Cmc1) plus oat (Avena sativa L.) as a nonhost. The two mite-resistant winter wheat lines, plus another mite-resistant backcross line with resistance from rye (Secale cereale L.) (Nst*5/1RS-1BL) and Norstar were also used as subplot treatments. The presence of vector resistance in the spreader treatments reduced the intensity of disease symptoms in the spreader rows themselves and increased their grain yield. In 2 of 3 yr, these yield differences were dramatic. Resistance in the spreader also reduced the secondary spread of WSM into the adjacent winter wheat subplots with conventional planting dates. During severe outbreaks of WSM, (1996-1997 and 1997-1998), Nst*5/Cmc2 was more effective with a lower frequency of severely infected plants and smaller yield losses than Nst*5/Cmc1 or Nst*5/1RS-1BL. In conclusion, control of WSM through vector resistance requires an effective resistance gene in both the spreader and the crop.
Abbreviations: Cmc1 etc, gene designations for resistance to "Curl mite colonization" • WSM, wheat streak mosaic • WSMV, Wheat streak mosaic virus
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INTRODUCTION
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WHEAT STREAK MOSAIC is a damaging viral disease of wheat in the Great Plains region of North America that causes yield losses that can exceed 60%. An outbreak of WSM in Alberta in 1964 was responsible for yield losses of 24.7 million L (700 000 bu) of winter wheat (Atkinson and Grant, 1967). In Kansas, WSM caused an average annual yield loss of 546 million L (15.5 million bu) between 1987 and 1991 (Harvey et al., 1994).
This disease is caused by Wheat streak mosaic virus (WSMV), which is spread by the wheat curl mite (WCM), Aceria tosichella Keifer, syn. Aceria tulipae Keifer (Slykhuis, 1955). Mite-susceptible wheat cultivars respond to mite colonization by rolling at the leaf margins. This provides a protected environment for the mites to lay eggs and increase their populations. Mites acquire WSMV as they feed on infected plants; they can then transmit the virus for a further 6 to 9 d (Paliwal and Slykhuis, 1967).
While the long-term reservoir of virus and vector is the native grasses (Christian and Willis, 1993), disease outbreaks are most common where viruliferous mites are wind dispersed from an infested crop or volunteer plants onto a nearby susceptible crop. WSM incidence is enhanced in areas where winter wheat and spring wheat are both cultivated extensively (e.g., South Dakota, Montana) or where winter wheat is seeded early to provide fall grazing for cattle (e.g., Texas, Oklahoma). In these cases, WSM cycles either from over-summered wheat plants onto winter wheat crops in the fall or onto spring wheat crops from overwintered wheat plants in the spring (Slykhuis, 1955; Christian and Willis, 1993). Usually, WCM are spread in large numbers by the wind over distances of several hundred meters or less, so WSM outbreaks may be localized to single fields or field margins.
The earlier that wheat becomes infected the more damaging is the disease. Primary infection of winter wheat during the fall results in stunting and yield reduction in winter wheat (Slykhuis et al., 1957; Atkinson and Grant, 1967). The following spring, migration of viruliferous mites moves WSM further into the field of winter wheat, but results of this secondary spread are less severe. However, the same fields can provide primary inoculum for adjacent fields of spring wheat, with severe results. WCM rarely disperses over long distances in large numbers (>1–2 km), so if an infected field of spring wheat is remote from any population of overwintered plants, a nearby native reservoir of inoculum may be suspected (Christian and Willis, 1993).
WCM requires green plant material to survive and populations decline rapidly as the crop ripens (Slykhuis, 1955). WSM is controllable by preventing initial spread of the WCM onto young seedlings of the new crop (Slykhuis et al., 1957). Infected volunteers should be eliminated and adjacent maturing crops should be ripe before the new crop emerges. However, this is not always practical. Green bridges to winter wheat may trigger the disease if cool fall weather delays ripening in spring-seeded cereals (Atkinson and Grant, 1967) or green bridges to spring wheat may occur where cultivated or sprayed volunteers die less quickly than expected.
Deployment of mite-resistant cultivars of winter wheat is one means for reducing losses caused by WSM (Andrews and Slykhuis, 1956; Harvey and Livers, 1975). Current commercial cultivars of winter and spring wheat are generally susceptible to both the WCM and WSM (Friebe et al., 1996). Resistance to WCM has been transferred into wheat from related grass species and rye. The mite-resistance gene Cmc1 was located on chromosome 6DS from T. tauschii (Thomas and Conner, 1986; Whelan and Thomas, 1989; Thomas and Whelan, 1991). Cmc2 from the JS genome of Th. ponticum (Whelan and Hart, 1988; Chen et al., 1999) and mite-resistance from Haynaldia villosa (L.) Schur. (Chen et al., 1996) were also located on group 6 while a mite-resistance gene from rye was located on 1RS (Harvey and Livers, 1975). All four sources have been transferred to wheat. In addition, resistance has now been identified in common wheat itself (Harvey et al. 1995a).
Testing under controlled environmental conditions indicated that different mite resistance genes were not equally effective in reducing the spread of WSM (Conner et al., 1991). After exposure to viruliferous mites, germplasm carrying resistance derived from Th. ponticum had a lower incidence of WSM than wheat lines carrying mite resistance from either T. tauschii or rye. The present study was undertaken to compare the effectiveness of different sources of mite resistance in reducing the primary and secondary spread of WSMV and minimizing yield losses in the field by means of lines with a common genetic background.
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MATERIALS AND METHODS
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Naturally occurring outbreaks of WSM provided uniform exposure of the spreader rows to viruliferous mites in each year of a 3-yr study at a field site near Lethbridge, AB. The spreader row treatments were seeded in July to maximize exposure to viruliferous mites. The experiment was arranged as a split-plot design with six replications using spreader rows as the main plot treatments and winter wheat lines seeded in early September as subplot treatments. In the first year of the study, the spreader row treatments included the mite-susceptible CDC Kestrel, the mite-resistant Nst*5/Cmc2 (a Norstar-derived backcross line carrying Cmc2) and the nonhost crop oat. In the last 2 yr of the study, Norstar replaced CDC Kestrel as the mite-susceptible spreader row and the mite-resistant Nst*5/Cmc1 was added as a fourth spreader row treatment. Spreader treatments (main plots) were seeded in blocks of five (1996) or four (1997 and 1998) 1- by 6-m plots per replicate. A 1-m space was left between these spreader plots to allow for the later seeding of subplot treatments. To reduce interference between main plots, these were completely surrounded with the nonhost (oat) also seeded at this time.
The subplot treatments included Norstar, Nst*5/Cmc1 and Nst*5/Cmc2. The mite-resistant wheat-rye translocation line Nst*5/1RS-1BL, (a Norstar-derived backcross line carrying wheat curl mite resistance from the 1RS-1BL Robertsonian translocation present in the ‘Chinese Spring’ derivative ‘Salmon’ via the line KS80H4200), was included as a subplot treatment in the first year of the study. Subplot treatments were seeded in mid September in 1- by 6-m plots in the spaces between the spreader plots.
Each summer, the severity of WSM was rated when the subplot treatments were at the soft dough stage (Growth Stage 85, Zadok et al., 1974). The plants were visually categorized as either healthy (no symptoms), moderately diseased (faint to obvious mosaic often with minor stunting), or severely diseased (strong mosaic–yellowed–dead, heavily stunted). Disease severity in the spreader row treatments was determined based on 40 and 20 plant samples taken from an end of the plot in the first year and two subsequent years, respectively. No data were taken from the oat spreader rows, as these did not survive the winter. In the first year of the study, 100 plants from one end of each plot of the subplot treatments were examined to determine disease severity. In the last 2 yr, disease severity in the subplot treatments was determined on the basis of a 50-plant sample taken from the end of each plot. Grain yield was determined by harvesting a 1- by 3-m area of each of the plots of the spreader rows and subplot treatments. Since the nonhost spreader treatment did not survive the winter, subplot yields in this treatment may be biased upward by reduced competition at the margin. Our conclusions have taken this into account.
Bartlett's test for homogeneity of the variance (Snedecor and Cochran, 1976) indicated that the data from this study did not require transformation. A multiyear analysis of variance showed that disease and yield responses were not fully consistent over years. Therefore, data from each year of the study were analyzed separately by means of appropriate models. Each year, the means of spreader row treatments, cultivars, and subplots within the spreader row treatments were compared by Fisher's Protected LSD test at the 5% level of significance (Steel and Torrie, 1980). Data from the spreader rows themselves were also analyzed. All statistical tests were performed with SAS (SAS, 1989). All conclusions drawn in the results section are statistically significant (P < 0.05) unless stated otherwise.
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RESULTS
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Disease Ratings and Yield Levels
Moderate and severe WSM symptoms were negatively correlated with each other where the disease was severe (–0.69, –0.34, and –0.72 in subplots in 1997 and 1998 and in the spreaders; data from Tables 1–3), but showed positive correlation (0.32) where the disease was lighter (subplots in 1999; data from Table 4). Since the number of plants with moderate symptoms was low and relatively constant compared with the other two classes (no symptoms and severe symptoms), the negative correlation between the mean frequency of plants with severe symptoms and plants with no symptoms was extremely high. For the spreader plots (Table 1), this correlation was –0.94, while for the yield plots (Table 2), correlations of subplot means by year ranged from –0.98 to –0.99 showing that these two variables were the inverse of one another despite existence of the moderate class. Therefore, only the incidence of severe symptoms was considered further.
1996–1997 Spreader
Judging from symptoms observed in the following summer, disease pressure which developed in the early-seeded (July) spreader row treatments was high (Table 1). About 98% of plants in the mite-susceptible wheat spreader row plots (CDC Kestrel) showed severe WSM symptoms. In the mite-resistant spreader Nst*5/Cmc2, 54% of plants had severe WSM symptoms and so this line out-yielded the susceptible spreader (CDC Kestrel) by a factor of 3. Plants of the oat (nonhost) spreader did not survive winter, so these were neither rated nor provided any yield.
1996–1997 Subplots
Variation in the transfer of WSM from the early-seeded spreader rows to the conventionally seeded subplots (planted in September) (Table 2), created a significant negative correlation between the mean yield of the various cultivar x spreader treatments and their mean incidence of severely diseased plants (r = –0.86, df = 6; oat subplots omitted). Mean disease ratings were lowest for plots grown adjacent to the nonhost spreader row treatment (oats). This was followed by plots exposed to resistant spreader (Nst*5/Cmc2) and then the susceptible spreader (CDC Kestrel). Plots adjacent to resistant wheat spreader outyielded plots adjacent to susceptible wheat spreader in line with their higher symptoms. Across subplot treatments, the three resistant lines out-yielded their susceptible recurrent parent and had fewer plants with severe WSM symptoms. WSM symptoms were lowest in the Nst*5/Cmc2 backcross.
1997–1998 Spreader
Disease pressure from the early seeding of the spreader row treatments was most intense in the second year of the experiment (Table 1). Regardless of the presence of mite resistance, all wheat spreaders exceeded 90% of plants with severe virus symptoms. These included mite-resistant backcrosses carrying Cmc1 and Cmc2 plus their mite susceptible recurrent parent Norstar. As a consequence of high disease levels, yields of the spreader plots were very low. Nonetheless, there were differences in yield among the spreader row treatments and these were proportional to the small number of less-affected and unaffected plants which remained (Table 1; Nst*5/Cmc2>Nst*5/Cmc1 >Norstar).
1997–1998 Subplots
As in the previous year, variation in the transfer of WSM from the spreader rows to the subplot treatments, produced a negative correlation between the yield and the mean number of severely affected plants (r = –0.68, df = 7;oat subplots omitted). As in 1996–1997, expression of WSM symptoms was lowest in subplots grown adjacent to nonhost oat spreader. Mite resistance in the wheat spreader reduced the incidence of severe WSM symptoms in subplots compared with subplots with susceptible wheat spreader but corresponding differences in yield were insignificant. Averaged across the spreader treatments, among the lines present in the subplots, Nst*5/Cmc2 yielded best, followed by Nst*5/Cmc1 and then Norstar. The reverse order was noted in the incidence of severe WSM symptoms (Nst*5/Cmc2<Nst*5/Cmc1<Norstar) although the difference between Nst*5/Cmc2 and Nst*5/Cmc1 was not significant.
1998–1999 Spreader
Compared with the previous 2 yr, disease pressure in the wheat spreader row treatments was not as strong (Table 1). While the incidence of severely affected plants was highest in the susceptible variety Norstar and resulted in the lowest yield, its yield as a spreader still exceeded 4 Mg ha–1 with 20% of plants escaping the disease (no symptoms of WSM).
1998–1999 Subplots
In 1999, the incidence of severe WSM symptoms in the subplots with nonhost (oat) spreader (21.9%) was comparable with those in 1997 and 1998 (21.9 vs. 24.1 and 26.7%). By contrast, disease incidence for the subplots with susceptible wheat spreader was low in the third year compared with the first 2 yr (22.5% vs. 71.2 and 69.0). Clearly, differences in the transfer of WSM to the subplots based on the mite reaction of the spreader, which were observed in Years 1 and 2, were not evident in the final year of the experiment (Table 4). No significant correlation existed between the incidence of severely diseased plants and yields of the subplot treatments (r = 0.28, df = 7; oat subplots omitted). Subplot yields showed that the mite-resistant line Nst*5/Cmc2 out-yielded both the line Nst*5/Cmc1 and Norstar. However, WSM ratings showed fewer severely affected plants in Nst*5/Cmc1 than in Nst*5/Cmc2, which in turn was lower than Norstar. This trend was recorded independently across each of the four different spreader treatments (Table 4); it strongly suggests a change in the ranking of gene effectiveness occurred in 1999, placing Nst*5/Cmc1 over Nst*5/Cmc2 (Tables 1, 2, and 3; see also Conner et al. 1991).
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DISCUSSION
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Mite Resistance and Disease Control
Under favorable conditions for an outbreak of WSM, mite-resistant winter wheat planted as the crop decreased spread of this disease and out-yielded susceptible winter wheat, thus demonstrating that vector resistance can reduce the spread of WSM from nearby sources. In addition, spread of the virus by the vector was also reduced when the source of the infestation also contained mite resistance (Tables 1–4). Differences were noted in the efficacies of the mite resistance. Under severe disease pressure, the mite resistance gene from Th. ponticum (Nst*5/Cmc2) was more effective than the gene from Aegilops squarrosa L. (Nst*5/Cmc1) or from rye (NST*5/1RS-1BL). These effects on the development of WSM symptoms in the various sources of resistance in near-isogenic materials grown in the field confirm the differences previously reported by Conner et al. (1991) in a controlled environment and among nonisogenic backgrounds. However, this was reversed under light disease pressure in 1999 where Nst*5/Cmc1 showed a lower incidence of symptoms than did Nst*5/Cmc2. In general, the data showed that some vector resistances control the disease more effectively than others and that vector resistance will be needed in both spreader and crop to approach the level of protection that is afforded by a nonhost spreader.
Design Considerations and Plot Size
In a prior study (1994–1996), an attempt was made to study these same factors in a location isolated by grassland. The approach taken was to study in large plots the gradient of infection originating from a strip of an artificially infested spreader. Difficulties encountered included soil variability within and between the large plots, light infestation, soil erosion, winterkill, and infestation by western wheat aphid [Diuraphis tritici (Gillette)]. A new design was adopted in 1996–1997, on the basis of the following considerations: surrounding the main plots with oat halted soil erosion and reduced interference among the main plots; the smaller experimental scale reduced field variability and lowered the risk of trapping the relatively rare western wheat aphid within the confines of the experiment; the high ratio of spreader to crop trapped enough wild mites to substitute for artificial infestation. Despite the fact that oat support few or no WCM, the presence of severely diseased plants in subplots with nonhost spreader shows that the main plots were not sufficiently well separated to eliminate interplot interference by the vector. Interference is a well recognized problem that was noted in previous studies with WSM (Slykhuis et al., 1957), but the scale at which it completely disappears may be too large for practical experimentation. Despite some interference, our findings were repeatable in relatively small plots and will be more effective when implemented at field scale.
The Outlook for Resistant Cultivars
Mite resistance was originally considered for disease control in winter wheat because it had the potential to prevent the spread of WSM and Wheat spot mosaic (Slykhuis, 1956), which are both vectored by the WCM. Difference in the virulence of different strains of WSMV (Carroll et al., 1982) also posed a problem in developing winter wheat lines with stable WSMV resistance. More recently, the High plains virus was recognized as a new important pathogen of wheat and other cereal crops that is also vectored by the WCM (Mahmood et al., 1998; Seifers et al., 1997). The development of mite-resistant cultivars should help prevent outbreaks of all three of these diseases.
Development of mite-resistant winter wheat cultivars at Lethbridge has involved a long-term commitment of time and resources. The mite vector was first identified and vector resistance first demonstrated in the 1950s, but our first cultivar with mite resistance (AC Radiant with Cmc1) was released to seed growers in 2001. Further deployment of mite resistance may now be complicated by the possibility of evolution in the mite. Following the widespread popularity of TAM 107 in Kansas and adjoining states, Harvey et al. (1995b)( 1997) recovered strains of the WCM which were adapted to the mite resistance gene from rye that is present in this cultivar. Later Harvey et al. (1999) reported that strains of the WCM, which could overcome the mite resistance conferred by Cmc1 and Cmc2 were common in counties in Kansas as well as in five U.S. states and Alberta. This is surprising, since neither Cmc1 nor Cmc2 have been deployed in commercial winter wheat cultivars. Our data shows that both genes can offer significant control of WSM. At the same time it is noted that the reversal between Cmc1 and Cmc2 could be explained by emergence of a mite strain virulent on the latter in 1998–1999. Additional information is needed to determine the prevalence and fitness of virulent strains of the WCM, the breadth of their virulence on various resistance genes and their potential for causing WSM outbreaks in mite-resistant winter wheat under field conditions.
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ACKNOWLEDGMENTS
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The authors thank David H. Quinn, Allan D. Kuzyk, Martin O. Fast, Tara L. Curtis, Kerry L. Kettle, Gayle L. Luca, Crystal L. Pierson, Tara E. Smith, and Jennifer N. Tacaks for their technical assistance in this study. We gratefully acknowledge the financial support received from the Canadian Wheat Board checkoff administered by the Western Grains Research Foundation and the Matching Investment Initiative of Agriculture and Agri-Food Canada. We also thank Gerald C. Kozub and Brian Nishiyama for their assistance in the statistical analysis of this study and Brian Beres for field operations.
Received for publication August 13, 2002.
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REFERENCES
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- Andrews, J.E., and J.T. Slykhuis. 1956. Reaction of winter wheat varieties and Triticum x Agropyron hybrids when inoculated with wheat streak mosaic virus by the mite vector Aceria tulipae Keifer. Plant Dis. Rep. 40:513–516.
- Atkinson, T.G., and M.N. Grant. 1967. An evaluation of streak mosaic losses in winter wheat. Phytopathology 57:188–192.
- Carroll, T.W., S.K. Zaske, and R.H. Brlansky. 1982. Separation of Montana isolates of wheat streak mosaic virus of Michigan Amber wheat. Plant Dis. 66:916–918.
- Chen, Q., R.L. Conner, and A. Laroche. 1996. Molecular characterization of Haynaldia villosa chromatin in wheat lines carrying resistance to wheat curl mite colonization. Theor. Appl. Genet. 93:679–684.
- Chen, Q., R.L. Conner, A. Laroche, G. Fedak, and J.B. Thomas. 1999. Genomic origins of Thinopyrum chromosomes specifying resistance to wheat streak mosaic virus and its vector, Aceria tosichella. Genome 42:289–295.
- Christian, M.L., and W.G. Willis. 1993. Survival of wheat streak mosaic virus in grass hosts in Kansas from wheat harvest to fall wheat emergence. Plant Dis. 77:239–242.
- Conner, R.L., J.B. Thomas, and E.D.P. Whelan. 1991. Comparison of mite resistance for control of wheat streak mosaic. Crop Sci. 31:315–318.[Abstract/Free Full Text]
- Friebe, B., K.S. Gill, N.A. Tuleen, and B.S. Gill. 1996. Transfer of wheat streak mosaic resistance from Agropyron intermedium into wheat. Crop Sci. 36:857–861.[Abstract/Free Full Text]
- Harvey, T.L., and R.W. Livers. 1975. Resistance to wheat curl mite, Aceria tulipae Keifer, in rye and wheat-rye addition lines. Environ. Entomol. 4:523–526.
- Harvey, T.L., T.J. Martin, and D.L. Seifers. 1994. Importance of plant resistance to insect and mite vectors in controlling virus diseases of plants: Resistance to the wheat curl mite (Acari: Eriophyidae). J. Agric. Entomol. 11:271–277.
- Harvey, T.L., T.J. Martin, and D.L. Seifers. 1995a. Survival of five wheat curl mite, Aceria tosichella Keifer (Acari: Eriophyidae) strains on mite resistant wheat. Exp. Appl. Acarol. 19:459–463.
- Harvey, T.L., T.J. Martin, D.L. Seifers, and P.E. Sloderbeck. 1995b. Adaptation of wheat curl mite (Acari: Eriophyidae) to resistant wheat in Kansas. J. Agric. Entomol. 12:119–125.
- Harvey, T.L., T.J. Martin, D.L. Seifers, and P.E. Sloderbeck. 1997. Changes in virulence of wheat curl mite detected on Tam 107 wheat. Crop Sci. 37:624–625.[Abstract/Free Full Text]
- Harvey, T.L., D.L. Seifers, T.J. Martin, G. Brown-Guedira, and B.S. Gill. 1999. Survival of wheat curl mites on different sources of resistance in wheat. Crop Sci. 39:1887–1889.[Abstract/Free Full Text]
- Mahmood, T., G.L. Hein, and S.G. Jensen. 1998. Mixed infection of hard red winter wheat with high plains virus and wheat streak mosaic virus from wheat curl mites in Nebraska. Plant Dis. 82:311–315.
- Paliwal, Y.C., and J.T. Slykhuis. 1967. Localization of wheat streak mosaic virus in the alimentary canal of its vector Aceria tulipae Keifer. Virology 32:344–353.[Medline]
- SAS Institute. 1989. SAS/STAT use's guide, Version 6, 4th ed. SAS Institute Inc. Cary, NC.
- Seifers, D.L., T.L. Harvey, T.J. Martin, and S.G. Jensen. 1997. Identification of the wheat curl mite as the vector of the high plains virus of corn and wheat. Plant Dis. 81:1161–1166.
- Slykhuis, J.T. 1955. Aceria tulipae Keifer (Acarina: Eriophyidae) in relation to the spread of wheat streak mosaic. Phytopathology 45:116–128.
- Slykhuis, J.T. 1956. Wheat spot mosaic, caused by a mite-transmitted virus associated with wheat streak mosaic. Phytopathology 46:682–687.
- Slykhuis, J.T., J.E. Andrews, and U.J. Pittman. 1957. Relation of date of seeding winter wheat in southern Alberta to losses from wheat streak mosaic, root rot and rust. Can. J. Plant Sci. 37:113–127.
- Snedecor, G.W., and W.G. Cochran. 1976. Statistical methods. 6th ed. Iowa State University Press, Ames.
- Steel, R.G.D., and J.H. Torrie. 1980. Principles and procedures of statistics. 2nd ed. McGraw-Hill Book Co., New York.
- Thomas, J.B., and R.L. Conner. 1986. Resistance to colonization by the wheat curl mite in Aegilops squarrosa and its inheritance after transfer to common wheat. Crop Sci. 26:527–530.[Abstract/Free Full Text]
- Thomas, J.B., and E.D.P. Whelan. 1991. Genetics of wheat curl mite resistance in wheat: Recombination of Cmc1 with the 6D centromere. Crop Sci. 31:936–938.[Abstract/Free Full Text]
- Whelan, E.D.P., and G.E. Hart. 1988. A spontaneous translocation that transfers wheat curl mite resistance from decaploid Agropyron elongatum to common wheat. Genome 30:289–292.
- Whelan, E.D.P., and J.B. Thomas. 1989. Chromosomal location in common wheat of a gene (Cmc1) from Aegilops squarrosa that conditions resistance to colonization by the wheat curl mite. Genome 32:1032–1036.
- Zadok, J.C., T.T. Chang, and C.F. Konzak. 1974. A decimal code for growth stages of cereals. Weed Res. 14:415–421.
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ABSTRACT
INTRODUCTION
