Previous PageTable Of ContentsNext Page

Soil-borne disease suppression of Rhizoctonia root rot in soils of the Eyre Peninsula, South Australia

Rowena Sjaan Davey1, Ann McNeill1 and Steve Barnett2

1Soil & Land Systems School of Earth & Environmental Sciences, The University of Adelaide, Waite Campus. rowena.davey@adelaide.edu.au
2
Plant and Soil Health, SARDI, Waite Campus.

Abstract

Soil-borne disease suppression is the ability of a soil to host a pathogen but not necessarily cause disease in crop. This form of disease suppression is likely to be driven by both abiotic (physical) and biotic (biological) soil characteristics. Eyre Peninsula (EP) soils in South Australia are considered to have many biotic and abiotic constraints which might inhibit the development of adequate levels of soil-borne disease suppression. However, with the adoption of management techniques such as stubble retention and increased yields through better nutrition it is possible that some soils on EP may become more suppressive. Pot experiments using three soils sampled from different paddocks on EP and a known suppressive soil (Avon) showed that the biotic factors of each of the three EP soils did not suppress Rhizoctonia in their own soil matrix, although the biotic factors from one of the three EP soils was able to confer suppression to Rhizoctonia when inoculated into the Avon soil abiotic matrix. However, the Avon biotic factors suppressive to Rhizoctonia were not successfully transferred to the abiotic matrix of any of the three EP soils suggesting the abiotic environment of EP soils inhibited disease suppression.

Key Words

Rhizoctonia solani, crop rotation, soil ecology

Introduction

The adoption of conservation tillage farming systems and direct drilling in recent years has increased the severity and extent of Rhizoctonia root rot in Australia (Rovira 1986). The Eyre Peninsula (EP) in South Australia (SA) is a region particularly vulnerable to Rhizoctonia disease incidence. While the EP produces approximately 40% of the SA wheat crop it has been estimated that Rhizoctonia root rot could reduce the yield in the northern part of this region by up to 60% (Crouch et al. 2005). Roget reported the decline in yield loss due to Rhizoctonia root rot at a long term trial site at Avon in SA. Further investigations led to the hypothesis and confirmation that this was due to biological factors within the soil (Wiseman et al. 1996). Disease suppressive soils are defined as “soils in which the pathogen does not establish or persist, establishes but causes little or no damage, or establishes and causes disease for a while but thereafter the disease is less important, although the pathogen may persist in the soil.” (Baker et al. 1974). A key question is whether the suppression developed at Avon can be obtained in other places, for example the upper EP where the soils are considered to be relatively ‘hostile’ to plant and soil organism function (Coventry et al. 1998). Thus, the specific aims of this work were to investigate (i) the inherent disease suppression to Rhizoctonia solani in the Avon and selected EP soils (ii) whether the suppressive organisms from Avon can be transferred successfully into autoclaved EP soils (iii) whether rhizosphere organisms from the EP soils can be transferred and cause suppression in autoclaved Avon soil .

Materials and Methods

Soils were collected in 2006 from 3 farmer paddocks on the upper EP in SA; near Minnipa (32 49. 797’S, 135 08.695’E), Mudamuckla (32 11.058’S, 134 04.770’E) and Streaky Bay (32 48 956’S, 134 10.175’E). Another soil was collected from the long term rotation trial (Roget 1995) at Avon in early 2007. Several kilograms of each soil were collected by random sampling the top 10cm across the paddock and these soils were bulked, air dried and sieved (2mm). All soil for the experiment, except those used to obtain “rhizo-biology” inoculum, were autoclaved twice in 48 hours, i.e. for one hour at 121C, 24 hours apart.

Two types of inoculum were used in this work, the “rhizo-biology” and the pathogen Rhizoctonia solani AG-8 as described by Barnett et al. (2006). Briefly, the “rhizo-biology” inoculum consisted of dried 14 day old wheat roots grown in each of the non-sterile soils plus the adhering rhizosphere soil. Rhizoctonia solani AG-8 inoculum consisted of two x 10mm Rhizoctonia solani infested agar plugs per pot. Bioassays were carried out in 300ml pots filled with 300g of air-dried soil and a known amount of sterilised RO water to achieve a wet weight of 75-85% field capacity which was maintained for the duration of the experiment. Surface sterilised and pre-germinated wheat seeds were planted into each pot and five seedlings grown for 28 days at 15C with a 12 hour night/day light regime. At sampling, the root and soil mix was removed from each pot, gently shaken to remove as much loose soil as possible and then the roots were washed with water to remove all remaining soil particles. Shoots were cut at the base of the stem and dried in an oven for four days at 60C after which dry weights were recorded. Roots were stored in a freezer prior to being rated for disease incidence. Disease incidence was described by a quantitative measure of percentage root infection (PRI), which was an assessment of the number of seminal roots truncated before 10cm and the number of roots showing signs of infection before 10cm (Barnett et al. 2006), calculated as:

Following disease rating roots were dried in an oven for four days and dry weights recorded.

The experiment was set out as a randomised block design with four replicates. There were two control treatments, the disease control consisting of autoclaved soil inoculated with pathogen and the healthy control comprising autoclaved soil alone. Experimental treatments were (1) inoculation of a soil specific “rhizo-biology” back into that same soil after it had been autoclaved, (2) inoculation of the Avon “rhizo-biology” into each of the other autoclaved soils and (3) inoculation of each soil specific “rhizo-biology” into autoclaved Avon soil. Pathogen inoculum was added to all of these treatments. For all the measures of disease incidence and plant growth, comparisons across different soils were made by representing the parameter as a % of the disease control within each replicate, while comparisons within each soil type were made using the original data values. Data was analysed as ANOVA, RCBD using GenStat Eighth Edition. Least significant difference (l.s.d.) at P=0.05 was used for comparison of treatment means.

Results

Disease and healthy controls

Table 1 Mean % root infection, root score, root and shoot dry weights (mg) for healthy and disease controls grown in the four soils used in this experiment (n=4).

*n=3, n.s. is not significant at p<0.05

Percentage infection for the disease controls was not significantly different, but was highest in the Minnipa soil, and decreased in the order Mudamuckla soil>Avon soil>Streaky Bay soil (Table 1). Shoot dry weight for the disease control in Avon soil was significantly higher than for the other three soils which decreased in the order Minnipa> Streaky Bay> Mudamuckla (Table 1). The Avon soil disease control had the highest dry root weight, followed by Mudamuckla, Streaky Bay and lastly Minnipa, although there were no significant differences.

Avon soil healthy controls had the highest root and shoot dry weights which were significantly different from all three of the EP soils (Table 1). Avon had a significantly higher root and shoot weight than all EP soils. Root weights for healthy controls in Mudamuckla and Minnipa soils were significantly greater than those in Streaky Bay soil, whereas shoot weights of healthy controls in Mudamuckla and Streaky Bay soils were significantly lower than those in Minnipa soil.

Treatment 1: Inoculation of soil specific “rhizo-biology” into its own autoclaved soil

Percentage root infection data from the treatment where each autoclaved soil was inoculated with its own “rhizo-biology” clearly shows a trend (not significant at p<0.05) for less disease in the Avon soil, since relative to the disease control there is about 40% less disease compared to a 10% decrease in all the EP soils (Table 2).

Treatment 2: Transfer of suppressive Avon “rhizo-biology” into all autoclaved soils

Inoculation of Avon “rhizo-biology” into Avon soil resulted in the lowest relative % root infection, approximately 40% less than the disease control. Relative % root infection for autoclaved Mudamuckla soil inoculated with Avon “rhizo-biology” was approximately 25% less than the disease control while inoculation of both Minnipa and Mudamuckla autoclaved soils with Avon “rhizo-biology” resulted in only a 10% decrease in % root infection relative to the disease control (Table 2).

Treatment 3: Inoculation of soil specific “rhizo – biology” into autoclaved Avon soil

Inoculation of “rhizo-biology” from Streaky Bay soil into Avon soil significantly (p<0.021) decreased mean % root infection compared to inoculation of “rhizo-biology” from Minnipa and Mudamuckla soils into Avon soil, and had a similar effect to Avon “rhizo-biology” in Avon soil (Table 2). Inoculation of Mudamuckla and Minnipa “rhizo-biology” into Avon soil resulted in similar mean % root infection values to the Avon soil disease control (Table 2).

Table 2: Percentage root infection relative to the disease control (value of 100%) for, inoculation of soil specific “rhizo-biology” back into its own soil (Treatment 1), inoculation of autoclaved soils with Avon soil “rhizo-biology” (Treatment 2); and percentage root infection after inoculation of soil specific “rhizo-biology” into the autoclaved Avon soil (Treatment 3). Different letters show significant differences at p<0.05, and n.s. no significant difference at p<0.05. All treatments were inoculated with Rhizoctonia solani AG-8.

Discussion

Variation in disease incidence between the disease controls highlights differences between each soil type in the ability of the soil abiotic environment to support pathogen survival and growth as well as to allow disease expression, defined as soil conduciveness towards that pathogen (Weller et al. 2002). The results suggest that Minnipa soil is the most conducive to Rhizoctonia solani, and Avon the least. However, as in this study, disease incidence is assessed as expression of the disease on a plant host and thus soil interactions involving the host also need to be considered. The healthy controls give some indication of impacts that each soil type has on the plant host and the results suggest that EP soils have lower inherent abiotic ability to support plant growth compared to Avon soil.

Although not significant, there is an indication that Avon “rhizo-biology” inoculated into its own abiotic soil environment is able to decrease disease incidence more than any one of the EP “rhizo-biology” in their own abiotic soil environments. This could be due to inherent differences in each soils “rhizo-biology”, due to an abiotic limitation within the EP soils, or a combination of both. .

The disease suppressive capacity of Avon soil was apparently not successfully transferred into EP soils, since disease incidence for these EP soils did not decrease after inoculation with Avon “rhizo-biology”. The lack of reduced disease incidence in EP soils supports the suggestion that an unfavourable abiotic environment exists that could be preventing suppressive organisms from fully functioning.

Disease incidence measures suggest that “rhizo-biology” from Streaky Bay soil is as suppressive as the Avon biological component. Combining these findings with the results of treatments 1 and 2, it could be suggested that Streaky Bay soil has a suite of organisms that are able to suppress disease but that there is some abiotic factor within Streaky Bay soil preventing the suppressive organisms from functioning to suppress disease.

Conclusions

Biotic factors of each of the three EP soils did not suppress Rhizoctonia in their own soil matrix, although the biotic factors from one of the three EP soils was able to confer suppression to Rhizoctonia when inoculated into the Avon soil abiotic matrix. However, the Avon biotic factors suppressive to Rhizoctonia were not successfully transferred to the abiotic matrix of any of the three EP soils. These results confirm and highlight the importance of the abiotic environment, the biotic component and their interactions on biological disease suppression and emphasise the need for further investigations.

Acknowledgements

Thank you to EPFS, SAGIT and GRDC for funding my scholarship and research. Thank you to A. Cook for the use of her data, W. Sheppard for collecting all the soil and S. Anstis for the Rhizoctonia. Thank you also to N. Wilhelm and K. Clarke for their support, discussions and advice and finally, thank you V. Gupta for assistance with this paper.

References

Baker, K. F. and R. J. Cook (1974). Biological control of plant pathogens. San Francisco, U.S.A., W.H. Freeman & Co.

Barnett, S. J., D. K. Roget, et al. (2006). Suppression of Rhizoctonia solani AG-8 induced disease on wheat by the interaction between Pantoea, Exiguobacterium, and Microbacteria. Australian Journal of Soil Research. 44: 331-342.

Coventry, D. R., R. E. Holloway, et al. (1998). Farming fragile environments: low rainfall and difficult soils in South Australia. 9th Australian Agronomy Conference, Wagga Wagga, Australia.

Crouch, J., B. Purdie, et al. (2005). Seed treatments for Rhizoctonia control. Eyre Peninsula Farming Systems 2005 Summary: 81 - 82.

Roget, D. K. (1995). "Decline in root rot (Rhizoctonia solani AG-8) in wheat in a tillage and rotation experiment at Avon, South Australia." Australian Journal of Experimental Agriculture 35(7): 1009 - 1013.

Rovira, A. D. (1986). "Influence of Crop Rotation and Tillage on Rhizoctonia Bare Patch of Wheat." Phytopathology 76(7): 669 - 673.

Weller, D. M., J. M. Raaijmakers, et al. (2002). "Microbial Populations Responsible for Specific Soil Suppressiveness to Plant Pathgens." Annual Review of Phytopathology 40(1): 309-348.

Wiseman, B. M., S. M. Neate, et al. (1996). "Suppression of Rhizoctonia solani anastomosis group 8 in Australia and its biological nature." Soil Biology and Biochemistry 28(6): 727-732.

Previous PageTop Of PageNext Page