Historically, P. sojae was first identified as a
soybean pathogen in the 1950's in Indiana, Ohio and North
Carolina. Resistance (Rps1) was also identified at
this time and incorporated into commercial cultivars (ie:
Harosoy 63 and Amsoy 71). As resistance has been deployed,
new races or pathotypes of P. sojae have developed.
Specifically in Ohio, during surveys in 1978-1980, P.
sojae race 3 (vir 1a, 7), race 7 (vir 1a, 3a, 7), and
race 9 (vir 1a, 6, 7) were the predominant races. During
1991, from 88 field samples it was determined that races 3,
7, 9 predominated, but 18 races, all with virulence towards
Rps-1k, were also identified. In preliminary surveys in
1997, from 16 locations in Ohio, an additional 14 new races
were identified that also had virulence to Rps-1k. P.
sojae races that have compatible interactions with many
of the deployed Rps genes have been identified in
many of the midwest states (Abney
et al., 1997; Leitz et al., 2000; Yang et al., 1996).
New sources of Rps resistance have been sought.
There have been several reports in which soybean germplasm
from China and South Korea have been evaluated for Rps
genes and some potential candidates have been identified.
However, the number of Rps genes, where they are
located on the soybean chromosome in relation to other Rps
genes has yet to be determined (Dorrance and Schmitthenner,
unpublished; Kyle et al., 1998; Lohnes et al., 1996).
Single gene resistance has been somewhat
"durable" at some level because soybean producers
have been planting cultivars with only a few Rps
genes and these genes have been effective for 8 to 15 years
(Schmitthenner, 1985). The longevity of Rps
resistance may be due to the nature of soil-borne diseases,
the dynamics of infection, subsequent inoculum production
and dissemination are limited within the soil environment.
There have been questions regarding the role of secondary
inoculum in epidemic development within any given season.
For disease management purposes, we treat this disease as
monocylic disease and focus our management efforts on the
inoculum that is present at planting. Most fields in Ohio
have adequate inoculum levels present to initiate an epidemic
(Miller et al., 1997). However, with the effectiveness of
single gene resistance in question in many regions of the
United States
other types of resistance are needed.
Partial resistance, (also termed field resistance,
rate-reducing resistance, general resistance, or tolerance), has been shown to be
effective against all races of P. sojae (Tooley and
Grau, 1982; Schmitthenner, 1985). In soybeans with partial
resistance, some root rot develops, but is limited (Tooley
and Grau, 1982; Schmitthenner, 1985). This resistance is
also thought to be rate-limiting (Tooley and Grau, 1982;
1984a; 1984b). Partial resistance in a number of host
pathogen interactions can be divided into components, ie.
specific attributes of the resistance such as reduced number
of infection sites, reduced lesion expansion, longer time
period for fungal reproductive structures to form as well as
reduced sporulation (Parlevliet, 1979).
The primary component of partial resistance to P.
sojae was the ability to restrict fungal colonization of
the plant tissue (Tooley and Grau, 1984a). Tooley and Grau
(1984a) reported from field evaluations, that area under the
disease progress curve, simple interest infection rate, and
disease incidence at growth stages V7 (late vegetative) and
R5 (beginning seed development) differentiated soybean
cultivars with varying degrees of rate-reducing resistance.
In addition, they found that differences in yield among
cultivars in P. sojae infested soil could be
attributed to the degree of rate-reducing resistance present
in the cultivar (Tooley and Grau, 1984b). In studies with
other soybean lines there is evidence that partial
resistance is highly heritable and a quantitative trait (Buzzell
and Anderson, 1982; St.Martin and Dorrance, unpublished;
Walker and Schmitthenner, 1984). In addition, St. Martin et
al. (1994) reported that partial resistance [tolerance]
should not negatively impact yield potential of soybean
cultivars.
| Currently, partial resistance is identified by
challenging soybean lines with a single compatible
(susceptible interaction) race to determine the amount of
the soybean plant that is colonized. In greenhouse assays, approximately 30% of the roots are
colonized by P. sojae in soybean cultivars with high
levels of partial resistance. Soybean plant introductions
with very high levels of partial resistance may contain
other types of resistance that cannot be identified with
these methods. There are reports from Ohio, Maryland and
Australia in which races of P. sojae have adapted to
cultivars which were believed to have high levels of partial
resistance(<20% roots colonized), but were subsequently identified as single major
genes expressed in the roots (McBlain et al., 1991; Ryley et
al., 1998; Thomison et al., 1988; Thomison et al., 1991). |
Figure 5. Greenhouse evaluations of soybean cultivars
with various levels of partial resistance, plants from
left to right are scored as follows: Control, 3.5, 4.5
and 6 on a scaled of 1 to 9, in which 1=no visible
root rot and 9=all plants are dead. |
| A
characterization of the reaction caused by Rps2
and other soybean lines that have a high degree of
partial resistance, or potentially other single major
genes for resistance, is necessary in order to avoid
selecting for these single genes. Field evaluations in
an area conducive to infection and subsequent disease
development with a diversity of races of P. sojae
is warranted.
|
Buzzell and Anderson (1982) proposed that selection for
partial resistance [tolerance] combined with Rps
genes would in fact provide long-term disease control of P.
sojae in soybeans. In order to preserve potentially
novel Rps genes they should ultimately be used in
combination with partial resistance. However, it is
necessary to identify how soybean cultivars, plant
introductions and populations with high levels of partial
resistance limit disease development under field situations
with a diverse population of P. sojae. This will
enhance our efforts to determine specific components of
partial resistance that limit disease development in the
field and will greatly assist in the rapid development,
deployment and appropriate utilization of this type of
resistance.
References
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