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New
Insights into the Make-up and Management of Soilborne Crop Pathogens Under
Driect Seeding : Rhizoctonia
Timothy
Paulitz
USDA-ARS, Root Disease and Biological Control Laboratory, Pullman, WA
Rhizoctonia bare
patch and root rot is caused by the fungus Rhizoctonia solani AG-8. Described
in Australia in the 1930s, this disease became a major problem in direct-seeded
wheat in Australia from the late 70s and was first discovered in the Pacific
Northwest in the mid 1980s (Weller et al. 1986). This fungus attacks the
root system, causing lesions and pruning of crown and seminal roots. The
cortex can be completely rotted away, leaving a sharp "spear tip"
at the end of a severed root. In its acute phase, this disease results
in patches of killed or stunted plants several meters across in a field.
However, it also has a chronic phase, where the infected plants may be
shorter or less vigorous than surrounding healthy plants, resulting in
a general unevenness of a stand and reduction in yield.
In the last 15 years,
a number of discoveries have been made about this disease in the Pacific
Northwest. I will briefly review these as background, and then cover some
of the newer insights into this disease.
- The acute phase
of the disease, with bare patches, can drastically limit yields. Yield
of affected plants in patches was half of that outside the patches (Pumphrey
et al. 1987).
- R. solani AG-8
survives best in living host tissue, and can survive on the roots of
volunteers and grassy weeds. When these weeds or volunteers were killed
with glyphosate a few days before planting, the pathogen was able to
build up inoculum on these dying weeds and then cause severe disease
in the crop sown into these dying plants (Smiley et al. 1992). In fact,
the herbicide glyphosate (Roundup) blocks a biochemical pathway involved
in plant defense against fungal pathogens. If the weeds were killed
2-3 weeks before planting, this "green bridge" of Rhizoctonia
was reduced because other microbes had time to decompose and outcompete
Rhizoctonia in the dying host tissue.
- This disease can
be exacerbated by lack of tillage and the disease can be especially
severe in direct-seeded crops (Roget et al. 1996, Weller et al. 1986,
Pumphrey et al. 1987, Smiley et al. 1996). Cultivation is thought to
break up hyphal networks or increase fragmentation of inoculum, reducing
its size and hence its inoculum potential. Tillage also may accelerate
drying of the soil or change the soil structure and influence microbial
activity suppressive to R. solani AG-8. However, most of these experiments
have been short term, and we do not know how direct-seeding affects
the disease over a longer time.
- There is no genetic
resistance to this disease in existing adapted cereal varieties in PNW,
based on extensive testing by researchers in Oregon and Washington over
the last 10 years.
- Seed treatments
are not effective against the patch version of this disease, and possibly
not against the chronic form. None of the available seed treatment fungicides
move systemically to the root. Several fungicides had activity against
R. solani in the lab, but were not effective in field trials (Smiley
et al. 1990). Biological seed treatments have shown some success in
the field, (Kim et al. 1997), but are not available commercially.
- There are very
few management strategies for this disease. Besides elimination of the
green bridge, Cook et al. (2000) and Roget et. al. (1996) have shown
that disruption of the soil in the seed zone during seed drilling and
proper placement of fertilizer in the seed band can reduce the severity
of the disease.
- Rhizoctonia can
decline in long- term cereal monocrop production. Lucas et al. (1993)
took soil cores from tilled and nontilled soils, infested them with
R. solani, and planted successive crops of wheat in the greenhouse.
After the 2nd or 3rd crop, the disease declined, and declined faster
in the tilled soil. MacNish (1988) found that Rhizoctonia declined to
almost nothing 7-9 years after continuous wheat in Australia. Roget
(1995) showed an increase in Rhizoctonia patch development over the
first 5 years of direct-seeded wheat, but then the disease declined
to negligible levels over the next 5 years.
CURRENT QUESTIONS
AND NEW INSIGHTS
Based on this work,
there are still a number of questions that need to be answered. I will
pose some of these questions, and outline some current research that is
addressing these needs.
- Is R. solani
AG-8 the only important Rhizoctonia? Another Rhizoctonia spp., R.
oryzae has been reported in PNW, but there is conflicting information
about its importance. Smiley and Uddin (1993) tested three isolates
of R. oryzae and one isolate of R. solani AG-8. They found that R. oryzae
did not cause root rot in natural soil at 19 or 23 C, but did at 27
C. Isolates of R. oryzae did not cause rotting of crown roots or limit
yields in inoculated field experiments on winter wheat. Based on these
results, they concluded that AG-8 was more important. Similarly, Ogoshi
et al. (1990) found that R. solani AG-8 was more pathogenic than R.
oryzae in pasteurized soil at 10 C, but the reverse was true at 20 C.
This was based on testing only 3 isolates of each species. R. solani
had a temperature optimum 5 C below R. oryzae. In a collection of 45
fields in 1986, R. oryzae was isolated more frequently than AG-8, making
up 45% of the isolates. Mazzola et al. (1996) tested 19 isolates of
R. oryzae from Pacific Northwest wheat fields, and found 12 that caused
damping-off and reduction in root numbers at 12 C in natural soil. AG-8
had no effect on seedling emergence or seminal roots, but 4 out of 8
isolates caused root rot on wheat. The take-home message is that a wide
variation in virulence may exist within species of Rhizoctonia, and
R. oryzae may be just as important as R. solani AG-8, even in cool soils.
To further answer this question, we conducted surveys in Eastern Washington
in 2000 and 2001 to see where these species were distributed.
Results:
R. solani AG-8 is very difficult to isolate from roots. We modified
a medium by adding 1 ppm benomyl and 100 ppm chloramphenicol to water
agar make it more selective. Barley or wheat plants were collected from
sites in the summer, 2000, and spring, 2001. Roots were washed and plated
on this medium. After 24 hrs, plates were examined under a dissecting
scope, and hyphae with characteristic morphology were transferred to
water agar and then potato dextrose agar for identification. Out of
100 sites on the Cunningham Agronomy Farm north of Pullman in 2000,
R. oryzae was isolated from 27 sites, but no R. solani AG-8 was isolated.
In 2001, R. oryzae was the predominate Rhizoctonia sp. isolated (Table
1).
- What is the
spatial distribution of these species of Rhizoctonia in a direct-seeded
field? With the acute bare patch phase, this can be easily visualized.
But the chronic phase is more difficult to map. A more import question
is: How does this distribution change over time? Do these patches grow
or remain in the same place? To answer these questions, Cook et al.
(2002) mapped bare patches of AG-8 on a 4-year rotation experiment on
an infested farm near Ritzville. I have been mapping R. oryzae on an
intensively sampled 90-acre farm on the Cunningham Agronomy Farm, using
sites established by GPS. Some of these results are reported in Paulitz
et. al. (2001).
Results:
In June 2000,
15 plants were dug from each of 100 GPS-referenced sites on the 90-acre
site on the Cunningham Agronomy Farm, which had been direct-seeded
with 'Baronesse' spring barley. Roots were washed, and crown and seminal
roots were counted, along with the number showing symptoms of infection
by Rhizoctonia. In July, five plants were sampled from each site and
roots were washed and plated on Rhizoctonia-selective medium to measure
actual root infection. Yield was taken from 2 X 2 m plots hand harvested
at each site (Huggins and Cook, unpublished). Data were subjected
to geostatistics to interpolate between the measured points, and maps
were constructed for the distribution of disease and yield parameters.
Yield showed a non-uniform distribution, ranging from 2500 to 6000
lbs per acre. The incidence of seminal root infection ranged from
30-80%, and the incidence of crown root infection ranged from 5-25%.
Both kinds of roots showed a non-uniform aggregated distribution for
distribution of infection. There was some agreement between the root
disease and yield maps in some cases, many of the areas that had high
disease levels had low yields, and vice-versa. These maps can be viewed
at http://www.plantpath.wsu.edu/cookchair. R. oryzae was only isolated
from 27 of the sites, primarily from the southwest corner of the field.
In 2001, the field was cropped with direct-seed spring and winter
wheat, along with smaller strips of spring and winter barley, spring
and winter canola, and spring and winter peas. Samples were taken
as in 2001, except that root systems were also scanned to be digitally
analyzed with computer software to calculate root-health parameters
such as root length and diameters. Of the 29 sites with R. oryzae
in 2001, 23 sites were new, yet the basic pattern of disease at the
scale of the farm remained. R. oryzae was also isolated from winter
canola and winter peas. Despite 3 years of direct-seeding at the Cunningham
farm, no explosive increase of Rhizoctonia disease has been observed,
and no bare patches have been seen.
In contrast, in a 4- year rotation experiment at Ron Jirava's farm
in Ritzville, bare patches developed in years 3 and 4 in both continuous
spring wheat, spring wheat after spring barley, spring barley after
spring wheat, and in the 1st and 2nd year of spring wheat after consecutive
plantings of safflower and mustard. Patches were also present in these
two broadleaf crops after cereals. The area of patches in wheat grew
from the 3rd to the 4th year. Seventy-three percent of the area in
the 4th year was the same that had been patches in the 3rd year, but
the remaining 27% of the area was newly expanded. Twenty-five percent
of the area that was patches in the 3rd year did not show patches
in the 4th year. This shows that all crops in these rotations were
susceptible to the patch syndrome caused by R. solani AG-8, and that
these patches grow and recede from one year to the next.
- What is the
relationship between severity of Rhizoctonia root rot and yield?
To answer this question, yields, root disease ratings, and pathogen
isolations were made at 100 GPS-referenced sites on the Cunningham Agronomy
Farm in 2000 and 2001. In another set of experiments, yields and disease
ratings of a number of accessions were examined in inoculated plots
at the Spillman Agronomy Farm by Jaya Smith, as part of her MS thesis
at WSU.
Results:
At the Cunningham
Agronomy Farm in 2000 (Fig. 1), there was a negative correlation between
yield and incidence of root infection caused by Rhizoctonia, but only
at sites with higher disease or pathogen levels. High disease sites
typically had roughly 20% less than the maximum yield. At sites with
low levels of disease, where the yields ranged from 2,500- 6,000 lbs/acre,
soil edaphic factors apparently caused the low yields. However, other
soil factors may be co-correlated with pathogen levels, and reduced
yields may be a result of a complex interaction between environmental
and biological factors.
Fig. 1. Correlation
between spring barley yield (lbs/acre X 10) and Rhizoctonia oryzae
(incidence of recovery from roots)
In comparing disease and yields of accessions of spring wheat planted
in field plots infested with R. solani AG-8, Jaya Smith found a significant
negative correlation between severity of root disease and yield (r=-0.44,
n=158), which accounted for 20% of the yield variation. The correlations
between heading date, protein and plant height were also significant,
but disease only explained 5% of the variation of these parameters.
Clearly, other soil, nutrient, and water factors interact together.
But, like the study at the Cunningham Agronomy Farm, disease levels
were relatively low and this makes it more difficult to detect significant
correlations. Nevertheless, cultivars in inoculated plots yielded
an average of 13% less than in non-inoculated plots, P= 0.001
- Do R. solani
AG-8 and R. oryzae attack other broadleaf crops, and therefore can crop
rotation be used as a management tool?
Results:
Recent works
indicates that R. oryzae may also attack broadleaf crops. R. oryzae
was isolated from spring canola at Lind and from peas and canola at
the Cunningham Agronomy Farm. In May 2001, a field of peas south of
Lewiston showed symptoms of root rot and stunting, but only on half
of the field previously direct-seeded to spring barley. R. oryzae
was isolated from the roots and caused severe damping-off of peas
in pasteurized soil. In natural soil, the pathogen caused root discoloration,
death of root tips, including spear-tipping, and a reduction in number
and length of secondary roots formed on the main tap root. This is
the first report of R. oryzae on a broadleaf crop. R. solani AG-8
was also shown to be pathogenic to peas, lentils and canola in greenhouse
tests. The lack of rotational control by canola and safflower (Cook
et. al. 2002) is a further indication that R. solani AG-8 can survive
and build up inoculum on broadleaf plants.
- Can residual
sulfonylurea herbicides from previous crops make sensitive plant-back
crops more susceptible to Rhizoctonia?
Results:
SU herbicides
such as Maverick (sulfosulfuron) and Olympus have been shown to reduce
yields of sensitive crops such as barley planted 18-22 months after
the application of the herbicide on wheat (Fig. 2). In the field,
plants are stunted, and show symptoms consistent with Rhizoctonia
infection. Smiley et al. (1992) demonstrated that another SU herbicide,
chlorosulfuron (Glean) increased was associated with increased Rhizoctonia
damage on winter wheat in Oregon, and could increase Rhizoctonia in
the greenhouse. In a number of plant-back trials conducted by McGregor,
Inc, of Colfax, the incidence of Rhizoctonia increased in spring barley
planted in plots previously treated with these herbicides (Paulitz
and Reinertsen, unpublished data). At two trials in Mockonema in 2001,
the herbicide Raptor or Clearfield (imazomox), caused significant
reductions in plant height of spring barley, which was associated
with a higher incidence of Rhizoctonia.
Figure 2
- How does tillage
affect R. oryzae and R. solani AG-8 over time?
To answer this question, Kurt Schoeder, a PhD student at WSU, has been
looking at disease in paired conventional tilled-directed grower fields
in summer 2001. These are sites adjacent to each other, where the direct-
seeded field has not been cultivated for 20, 12, or 3 years. He has
also set up experimental directed-seeded plots on conventional tilled
land, and conventional tilled plots on direct-seeded land, to see what
happens to diseases during the initial conversion period. At this time,
the results of 2001 are still being analyzed.
- Is there any
genetic resistance in other Triticum gene pools or Triticum relatives?
Are there differences in susceptibility among spring wheat varieties
or advanced breeding lines? These questions were addressed by Jaya Smith
as part of her MS thesis with Dr. Kim Kidwell.
Results:
Jaya Smith (2001)
screened 13 spring barley, 13 spring wheat cultivars, 72 synthetic
hexaploids and 4 Triticale cultivars for resistance to R. solani AG-8
in the greenhouse. In addition, she screened accessions of Aegilops
cylindrica and Dasypyrum villosum. Resistance was found only in D.
villosum, which was resistant or moderately resistant. No resistance
was found in spring wheat or spring barley cultivars or synthetic
hexaploids. Two isolates of R. solani AG-8 were used, which showed
significant differences in virulence, especially with D. villosum.
This is another indication that there is pathogenic diversity among
isolates of R. solani.
Conclusions:
Much still needs
to be learned about this disease complex, to provide better management
tools in direct-seeded cereals. Genetic resistance would be the best control
method, but the search is still ongoing for what is probably a complex
multigenic resistance that may be difficult to move into agronomically
acceptable varieties. Identification of biological factors underlying
a natural suppression in the field may also be helpful, especially to
determine why the disease is a major problem in some direct-seeded fields
and not others.
References
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W. F. and Christensen, N. W. 2002. Rhizoctonia root rot and wheat take-all
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