Diseases of soybean in Australia

Transcription

1 Diseases of soybean in Australia Malcolm Ryley 1 and Andre Drenth 2 1 Farming Systems Institute, Queensland Department of Primary Industries, Toowoomba 2 Cooperative Research Centre for Tropical Plant Protection, University of Queensland Introduction Over 20 diseases of soybean (Glycine max L.) have been recorded in Australia, but we still do not have the world s most serious disease, soybean cyst nematode caused by Heterodera glycines Ichinohe (Wrather et al. 1997). Some diseases in Australia are widespread, such as phytophthora root and stem rot (caused by Phytophthora sojae) and sclerotinia rot, whereas others have a restricted distribution (such as downy mildew, phomopsis seed decay and phytophthora root rot (caused by Phytophthora macrochlamydospora). Although resistance to the major diseases is desirable and in many cases available from overseas, the only pathogen for which resistance has been specifically targeted in Australia is P.sojae. Management options for the other diseases include one or more of the following clean seed, residue burial, fungicides and rotations. Phytophthora root and stem rot (Phytophthora sojae) Phytophthora root and stem rot is considered to be the most serious disease of soybean in Australia. It has been found in all of the major soybean growing areas of Australia except central and coastal Queensland, and has had a significant impact on yield in some regions, such as, the Lachlan Valley in recent years. The disease is favoured by poorly drained clay soils, but can occur on lighter soils if they are saturated for an extended period. Cultural practices, such as, crop rotation and improved drainage can minimise the impact of the disease, but resistance is the most effective option. Three types of resistance have been identified (Schmitthenner, 1999). The first, immunity, is controlled by one or more of the following genes, Rps 1a, 1b, 1c, 1d, 1k, 3a, 3b, 3c, 4, 5, 6 or 7 which confer(s) complete resistance to one or more races. The second, field resistance is controlled by one known gene Rps 2, and confers a high level of resistance to more than one race. The third type has been termed root resistance, but is only partly characterised. Breeding for resistance to P.sojae is complicated by the existence of pathogenic strains (races or pathotypes). There is evidence from both Australia and the United States that P.sojae exists in the soil as a diverse population consisting of a complex of races, many at low frequency (Schmitthenner, 1994; Ryley et al., 1998). The relative frequency of races in a particular region is determined to a large extent by the resistance genes in the soybean varieties that are grown, and also by the intensity of soybean cultivation. To the present time, 14 races of P.sojae have been identified in Australia, but only 8 of these have been found in commercial crops (Table 1), with the remainder found at field sites (including research stations) where disease nurseries are conducted. There is a distinct geographic distribution of races in Australia.

2 In southern Queensland only races 1 and 15 have been recorded, with a shift from dominance of race 1 to race 15 due to the relative susceptibility of Davis and Davis derived cultivars (which possess Rps2) to race 15 (Ryley and Obst, 1992). Race 1 was the only race recorded on the north coast of New South Wales up until 1993/94, and in inland northern New South Wales until the 1998/99 season, when race 15 was isolated from Davis-derived cultivars such as Manark and Centaur. No other races have been identified on commercial crops in this region, but 7 other races have been identified at Hermitage Research Station, Warwick, and race 2 has been found in trial plots at Narrabri. Table 1. Races of Phytophthora sojae identified in commercial soybean crops in Australia. Race Resistance gene Distribution 1 7 All 15 2, 3 a, 5, 7 All 2 1b, 7 Northern New South Wales 4 1 a, 1 c, 7 Central + southern NSW 25 1 a, 1 b, 1 c, 1 k, 7 Central + southern NSW 33 1 a, 1 b, 1 c, 1 d, 1 k, 6, 7 Southern NSW 46 1 a, 1 c, 3 a, 5, 7 Southern NSW 53 1 a, 1 b, 1 c, 3 a, 5, 7 Southern NSW Before 1989 the race composition in the irrigated growing areas of central and southern New South Wales was similar to that of southern Queensland. In 1990 race 4 was found on cvv. Lachlan and Ridley, both of which are thought to possess the Rps1a gene (Ryley et al., 1992), and until 1996 that race had replaced race 1 as the dominant race in the Lachlan, Murrumbidgee and Murray River valleys. Two other races, 46 and 53 were recorded in this region, but in both cases only one isolate had been found in commercial soybean crops. The cultivar Banjalong [narrow-leafed Calland x Williams 82(Rps1k)] was released specifically to replace cultivars grown in the Lachlan Valley which were susceptible to race 4. Race 25 was isolated from Banjalong in 1993/94 and was confined to one site in the Lachlan Valley up until 1997/98. Then it was found on Banjalong in one crop in the Collemabally Irrigation Area (CIA) of southern New South Wales. The incidence of this race in the CIA has steadily increased in subsequent seasons, with most crops surveyed in the 1999/2000 season being infected. Isolates of the previously unrecorded race 33 were also collected from Banjalong in the CIA (Table 1). The dynamics of races of P.sojae in different soybean growing areas of Australia are influenced by the cultivars grown in those areas. The change in race dominance in southern Queensland has been driven by the widespread use of cultivars carrying the Rps2 gene (Ryley and Obst, 1992), while the appearance of races 4 and 25 in southern New South Wales have been due to the release and intense cultivation of cultivars with a single gene for resistance (Rps1a and Rps1k respectively). Races of P.sojae in southern New South Wales are apparently becoming more complex, with the races being capable of defeating many genes. The results from the survey and race classification activities

3 indicate that knowledge of the geographical and temporal dynamics of P.sojae is vital for the ongoing development and release of phytophthora resistant varieties in Australia. Breeding for resistance offers the only long-term solution to the disease. The vast majority of current commercial soybean varieties growing in high risk Phytophthora areas possess only a single gene for resistance, or unknown gene(s). Gene pyramiding, in which 2 or more genes for resistance are incorporated into a breeding line can reduce the chances of new pathogenic races being selected. There are a number of combinations (such as, Rps1c+2, Rps1k+2) which we believe may be in QDPI, CSIRO or NSW Agriculture breeding lines. However, pyramided genes are difficult to identify using traditional techniques, and molecular technology offers one possible solution to these difficulties. Microsatellite primers for the Rps1, Rps2, and Rps3 loci have been synthesised by our collaborators at the CRC for Tropical Plant Protection. Three satellite markers (Satt009, Satt431 and Satt335) have been chosen which are linked to Rps1, Rps2 and Rps3 respectively. An analysis of 11 F4 inbred progeny lines ( ) between the parents Centaur (Rps2) and (Rps1k + Rps3), produced by Dr Andrew James, CSIRO indicates that 7 of the lines possess Rps1, 5 contain Rps2, 4 contain Rps3, and 2 possess all three resistance genes. All 44 progeny of this cross will be screened using the satellite markers and the results confirmed using traditional root inoculation tests. The Rps2 gene has been detected in the recently-released QDPI cultivar Jabiru, and in two promising lines from the G cycle of the QDPI recurrent selection program. The technology has now been optimised to such a degree that a capacity is present for routine screening of important breeding lines and new cultivars to detect phytophthora resistance genes, in particular Rps1, Rps2 and Rps3, derived from all breeding programs. Phytophthora root rot (Phytophthora macrochlamydospora) This pathogen was described by Irwin (1991), based on isolates collected from cv. Hampton at Indooroopilly, Brisbane in Stovold and Smith (1991) had reported the occurrence of a Phytophthora species on soybean on the north coast of New South Wales in 1985, and a reexamination of material by Stovold et al., (1996) showed that the pathogen had been P.macrochlamydospora. Yield losses in the order of 30% were reported, and outbreaks in later years, such as, 1993/94 have been just as damaging. The symptoms and soil conditions needed for infection are distinct from those of Phytophthora sojae. The characteristic stem lesions caused by P.sojae are absent from P.macrochlamydospora-affected plants, in which there is a distinct internal and external discolouration of the tap root and extensive lateral root rot. We have only ever found the disease in soybean crops which had been flooded for some days, whereas P.sojae does not necessarily require flooded soil for infection. The disease has never been found in commercial crops outside the north coast of New South Wales. Stovold et al., (1996) showed that there was a range of reactions in the cultivars he tested, but none of these are now widely grown in the region. They also demonstrated that many native legumes, such as, Indigofera hirsuta L., Crotalaria medicaginea Lamb, Desmodium varians (Labill.) Endl., and Glycine spp., are highly susceptible. It seems highly likely that

4 P.macrochlamydospora is a native fungus which survives on naturally-occurring legumes, causing little damage to these hosts, but occasional severe damage to soybean. The requirement for flooded soil for severe disease to occur means that the disease can be largely controlled by avoiding fields prone to prolonged waterlogging. Sclerotinia rot (Sclerotinia sclerotiorum) Sclerotinia rot has been recorded in most soybean-growing areas of Australia and tends to be a disease of crops with high yield potential. It is now considered to be the second most important disease in the north central United States (Wrather et al., 1994). Outbreaks of the disease tend to occur when flowering coincides with lower than normal temperatures (crop canopy temperatures <28ºC) and moist weather which favours sclerote germination, spore production and dispersal, and infection. Spores develop in small mushroom-like bodies which develop from germinated sclerotes, and are liberated during changes in relative humidity in the canopy. They must colonise a petal or leaf before they can infect, so lesions usually develop on the stems at nodes. The first sign of infection in a crop is the wilting and death of the uppermost leaves on a plant, but by then the stem lesion is usually well advanced, with abundant mycelial growth and the early stages of sclerote development. Lush vegetative growth, lodging, an early-closed canopy, overhead irrigation and growing soybeans in fields in which one of its many hosts, such as, sunflower, brassicas, and other legumes has been included in rotations, promotes the development of sclerotinia rot. Apart from the cultivar Manta, which was selected on the north coast for its higher level of tolerance, there is no known resistance in Australian cultivars to the pathogen. Consequently, management of the disease relies on agronomic practices which reduce the potential damage. Avoidance of fields with a history of sclerotinia, planting on wide rows to reduce in crop humidity, limiting overhead irrigation during flowering, and using seed free from sclerotes will assist in the management of the disease. Although fungicides are relatively effective, they must be applied at the very early stages of infection, but usually the disease is not seen until infection is well advanced. Penetration of the fungicide droplets through the canopy to the infection site is also an issue. Now that the inheritance of resistance to S.sclerotiorum has been characterised in 2 cultivars (Hoffman et al., 1999), there is potential to introduce sclerotinia-tolerant breeding material from overseas into locally adapted genotypes. Charcoal rot (Macrophomina phaseolina) Charcoal rot can be considered to be an endemic disease of soybean in Australia. It has a very wide host range, including most summer-grown crops and weeds. Research conducted in the late 1990 s (Fuhlbohm, unpublished data) proved that the fungus can survive in the roots of a range of common weeds without causing symptoms and killing infected plants. Symptoms of the disease on soybean are first observed after flowering, when plants rapidly wilt and die usually after a short period of heat and/or moisture stress. An orange discolouration just below the surface in the basal part of the stem has been associated with charcoal rot, and as the plant dies the inside of the stem turns a charcoal colour, with numerous minute black dots, which are the microsclerotia of the fungus. The microsclerotia are capable of long-term survival in the soil or in crop

5 residue. Although symptoms appear after flowering it is possible that infection may have occurred in the seedling stage and remained latent until after flowering, as has been demonstrated for charcoal rot of mungbean (Fuhlbohm, 1994). There is no known resistance in soybean to the pathogen, so management relies on good irrigation practices, effective weed control and avoiding fields which experienced severe charcoal rot in previous seasons. Rhizoctonia rot (Rhizoctonia solani) Rhizoctonia rot has been reported in soybeans mainly on the north coast of New South Wales and in the CIA and MIA in southern New South Wales. Populations in the soil consist of isolates belonging in different Anastomosis Groups, each of which has a different host range and optimum conditions for infection and survival. Rhizoctonia can attack from the seedling stage onwards, causing seedling damping-off, and later root lesions, root pruning and stunting. The pathogen can survive in residues and as sclerotes. There is no known resistance to the disease, so management relies on cultural practices to minimise residue carryover. Flooding and interrow cultivation has been reported to reduce disease levels. Rhizoctonia is a significant disease of many summer and winter crops in the CIA and MIA, but until the composition of populations of the pathogen, and their pathogenicity on the major crops is determined, management options will remain limited. Downy mildew (Peronospora manschurica) Downy mildew had been confined to the north coast of New South Wales until the 1998/99 season, when it was identified in many crops throughout southern Queensland. The disease appears as pale green-light yellow spots on the upper surfaces of leaves, and during moist weather a grey downy growth, consisting of spores on branched structures (conidiophores), appear on the lower leaf surfaces. Pods can also be infected, with the result that the seed coat can be covered with a white crust consisting of mycelium and resistant oospores. Downy mildew is of significance for export of soybeans because New Zealand requires seeds to be free from the disease. The reasons for the appearance of downy mildew in southern Queensland are unknown, but could be related to the use of downy-mildew infected seed in a few crops or the spread of the pathogen from native glycines during cool, moist weather. Despite the apparently high levels of infection in some cultivars in southern Queensland, there were no reports of significant yield losses. However, in more conducive environments there is some evidence for damaging yield losses (Desborough, pers. comm.). Seed intended for sowing in downy mildew free areas should be treated with a fungicide, and many commercial Australian cultivars have a high level of resistance to the pathogen. Pod and stem blight and seed decay (Phomopsis species) and purple seed stain (Cercospora kikuchii) Stovold and Smith (1991) identified pod and stem blight, and seed decay (caused by Phomopsis species), as the most common disease of soybeans on the north coast of New South Wales. It is rarely found in the other soybean growing areas of Australia, but growth areas such as the coastal sugarcane areas of central Queensland may be at risk. The disease occurs in seasons with prolonged rainfall and high humidity during the pod

6 filling and maturation stage, particularly after the yellow pod stage (R7), when affected plants turn yellow and small black dots appear on the stems and pods. Seed quality is reduced through seed cracking, discolouration and shrivelling and mould growth, leading to a reduction in vigour and storage life. There is scope for a breeding solution because resistance has been identified overseas (Kulik and Sinclair, 1999). Purple seed stain has been an intermittent problem for many years, but has been more common in recent years on some cultivars. Older varieties such as Davis have some resistance to purple seed stain. The disease causes a general light purple discolouration of leaves, often turning them leathery, and a purple stain on affected seed. The initial infection in a crop appears to be from spores on infected crop residues, which cause latent leaf infections, and which in turn act as sources for subsequent pod infection. According to overseas reports, the incidence of purple seed stain is related to the cumulative numbers of spores detected above crops, which is partly determined by the amount of infected residue; it is also considered that weather factors are not a limiting factor in seed infection (Schuh, 1999). Management of crop residues and the use of disease-free will assist in the management of both seed decay and purple seed stain. Acknowledgements We wish to thank Helen Mosetter, Neale Obst, Damian Herde and Kerry Brett for race classification of P.sojae, and numerous casual assistants for the molecular marker work. We also acknowledge the Grains Research & Development Corporation for their financial support. References Fuhlbohm, M.J. (1994). Studies on charcoal rot of mungbean. Honours thesis, Botany Department, University of Queensland. Hoffman, D.D. Nickell, A.D., Nickell, C.D., Diers, B.W., and Hartman, G.L. (1999). Inheritance of partial resistance to Sclerotinia sclerotiorum in soybean cultivars, AsgrowA2506 and Novartis S Soybean Genetics Newsletter 26: Online. Irwin, J.A.G. (1991). Phytophthora macrochlamydospora, a new species from Australia. Mycologia 83: Kulik, M.M., and Sinclair, J.B. (1999). Phomopsis seed decay. Pp in Compendium of Soybean Diseases (4 th Edition; Eds. G.L. Hartman, J.B. Sinclair and J.C. Rupe) APS Press, St Paul MN, USA. Ryley, M.J. and Obst, N.R. (1992). Race-specific resistance in soybean cv. Davis to Phytophthora megasperma pv. glycinea. Plant Disease 76: Ryley, M.J., Obst, N.R., Irwin, J.A.G., and Drenth, A. (1998). Changes in the racial composition of Phytophthora sojae in Australia between 1979 and Plant Disease 82: Ryley, M.J., Obst, N.R., and Stovold, G.E. (1991). A new race of Phytophthora megasperma pv. glycinea on soybean in Australia. Australasian Plant Pathology 20: Schmitthenner, A.F., Hobe, M., and Bhat, R., (1994). Phytophthora sojae races in Ohio over a 10-year period. Plant Disease 78:

7 Schmitthenner, A.F. (1999). Phytophthora rot. Pp In Compendium of Soybean Diseases, 4 th Edition (Eds. G.L. Hartman, J.B. Sinclair, J.C. Rupe). APS Press, St. Paul MN, USA. Stovold, G.E. and Smith, H.L.P. (1991). The prevalence and severity of diseases in the coastal soybean crop of New South Wales. Australian Journal of Experimental Agriculture 31: Stovold, G.E., Smith, H.L.P. and Priest, M.J. (1996). Occurrence of Phytophthora macrochlamydospora in New South Wales and its pathogenicity to some legume species. Australasian Plant Pathology 25: Schuh, W. (1999). Purple seed stain. Pp in Compendium of Soybean Diseases (4 th Edition; Eds. G.L. Hartman, J.B. Sinclair and J.C. Rupe) APS Press, St Paul MN, USA. Wrather, J.A., Anderson, T.R., Arsyad, D.M., Gai, J., Ploper, L.D., Pora-Puglia, A., Ram, H.H., and Yorinori, J.T. (1997). Soybean disease loss estimates for the top ten soybean producing countries. Plant Disease 81: