Suppression of fusarium wilt of carnation by Pseudomonas putida WCS358 at different levels of disease incidence and iron availability

Treatment with Pseudomonas putida WCS358r, a rifampicin‐resistant derivative of strain WCS358, significantly reduced fusarium wilt of carnation grown in rockwool if disease incidence was moderate, but not if disease incidence was high. Differences in disease incidence could intentionally be established by varying the inoculum density of the pathogen Fusarium oxysporum f. sp. dianthi (Fod). The effectiveness of disease suppression by WCS358r increased with decrease of inoculum density and consequently decrease of disease incidence. WCS358r and a Tn5 marked derivative of WCS358 (B243) reduced fusarium wilt of carnation most effectively if a low iron availability for the pathogen was established by adding unferrated or only partially ferrated ethylenediamine [di(o‐hydroxyphenylacetic) acid]. A Tn5 mutant of WCS358 defective in siderophore biosynthesis (JM218) did not reduce disease incidence. Siderophore production and inhibition of Fod by WCS358r in vitro decreased with increasing iron availability, supporting the more effective disease suppression by strains WCS358r and B243 at low iron availability. Siderophore‐mediated competition for iron was shown to be the mechanism of suppression of fusarium wilt of carnation by P. putida WCS358. Its effectivity was highest at a low iron availability and at a moderate disease incidence.     

Influence of Fusarium wilt toxin(s) on carnation cells

The influence of culture filtrates of Fusarium oxysporum f.sp. dianthi which causes Fusarium wilt was investigated on growth and viability of carnation tissue cultures and leaf segments. Culture filtrates of avirulent race 1 of this fungus did not affect calli and leaf segments of cultivars both susceptible and resistant to Fusarium wilt. However, culture filtrates of virulent race 2 decreased viability and suppressed growth of callus of the susceptible cultivar. In contrast, callus of the resistant cultivar showed resistance to the culture filtrates. The results of these experiments may provide information on methods of selection of new wilt resistant carnation varieties.Abbreviations A270 absorbance at 270 nm - 2,4-d 2,4-dichlorophenoxyacetic acid - CF-MCD culture filtrate of 16064 grown in MCD medium - MCD medium modified Czapeck-Dox medium - MS medium basal medium of Murashige and Skoog - MW molecular weight - PD medium potato dextrose medium - TTC 2,3,5-triphenyl tetrazolium chloride     

Effect of genotype and root colonization in biological control of fusarium wilts in pigeonpea and chickpea by Pseudomonas aeruginosa PNA1

Pseudomonas aeruginosa PNA1, an isolate from chickpea rhizosphere in India, protected pigeonpea and chickpea plants from fusarium wilt disease, which is caused by Fusarium oxysporum f.sp. ciceris and Fusarium udum. Inoculation with strain PNA1 significantly reduced the incidence of fusarium wilt in pigeonpea and chickpea on both susceptible and moderately tolerant genotypes. However, strain PNA1 protected the plants from fusarium wilt until maturity only in moderately tolerant genotypes of pigeonpea and chickpea. Root colonization of pigeonpea and chickpea, which was measured using a lacZ-marked strain of PNA1, showed tenfold lower root colonization of susceptible genotypes than that of moderately tolerant genotypes, indicating that this plant-bacteria interaction could be important for disease suppression in this plant. Strain PNA1 produced two phenazine antibiotics, phenazine-1-carboxylic acid and oxychlororaphin, in vitro. Its Tn5 mutants (FM29 and FM13), which were deficient in phenazine production, caused a reduction or loss of wilt disease suppression in vivo. Hence, phenazine production by PNA1 also contributed to the biocontrol of fusarium wilt diseases in pigeonpea and chickpea.     

The effect of <Emphasis Type="Italic">Gossypium</Emphasis> C-genome chromosomes on resistance to fusarium wilt in allotetraploid cotton

Fusarium oxysporum f. sp. vasinfectum (Fov) has the potential to become the most economically significant pathogen of cotton in Australia. Although the levels of resistance present in the new commercial cultivars have improved significantly, they are still not immune and cotton breeders continue to look for additional sources of resistance. The native Australian Gossypium species represent an alternative source of resistance because they could have co-evolved with the indigenous Fov pathogens. Forty-six BC₃ G. hirsutum × G. sturtianum multiple alien-chromosome-addition-line (MACAL) families were challenged with a field-derived Fov isolate (VCG-01111). The G. hirsutum parent of the hexaploid MACAL is highly susceptible to fusarium wilt; the G. sturtianum parent is strongly resistant. Twenty-two of the BC₃ families showed enhanced fusarium wilt resistance relative to the susceptible G. hirsutum parent. Logistic regression identified four G. sturtianum linkage groups with a significant effect on fusarium wilt resistance: two linkage groups were associated with improved fusarium wilt resistance, while two linkage groups were associated with increased fusarium wilt susceptibility.     

Effect of pseudobactin 358 production by Pseudomonas putida WCS358 on suppression of fusarium wilt of carnations by nonpathogenic Fusarium oxysporum Fo47.

Nonpathogenic Fusarium oxysporum Fo47b10 combined with Pseudomonas putida WCS358 efficiently suppressed fusarium wilt of carnations grown in soilless culture. This suppression was significantly higher than that obtained by inoculation of either antagonistic microorganism alone. The increased suppression obtained by Fo47b10 combined with WCS358 only occurred when Fo47b10 was introduced at a density high enough (at least 10 times higher than that of the pathogen) to be efficient on its own. P. putida WCS358 had no effect on disease severity when inoculated on its own but significantly improved the control achieved with nonpathogenic F. oxysporum Fo47b10. In contrast, a siderophore-negative mutant of WCS358 had no effect on disease severity even in the presence of Fo47b10. Since the densities of both bacterial strains at the root level were similar, the difference between the wild-type WCS358 and the siderophore-negative mutant with regard to the control of fusarium wilt was related to the production of pseudobactin 358. The production of pseudobactin 358 appeared to be responsible for the increased suppression by Fo47b10 combined with WCS358 relative to that with Fo47b10 alone.     

Effect of pseudobactin 358 production by Pseudomonas putida WCS358 on suppression of fusarium wilt of carnations by nonpathogenic Fusarium oxysporum Fo47.

Nonpathogenic Fusarium oxysporum Fo47b10 combined with Pseudomonas putida WCS358 efficiently suppressed fusarium wilt of carnations grown in soilless culture. This suppression was significantly higher than that obtained by inoculation of either antagonistic microorganism alone. The increased suppression obtained by Fo47b10 combined with WCS358 only occurred when Fo47b10 was introduced at a density high enough (at least 10 times higher than that of the pathogen) to be efficient on its own. P. putida WCS358 had no effect on disease severity when inoculated on its own but significantly improved the control achieved with nonpathogenic F. oxysporum Fo47b10. In contrast, a siderophore-negative mutant of WCS358 had no effect on disease severity even in the presence of Fo47b10. Since the densities of both bacterial strains at the root level were similar, the difference between the wild-type WCS358 and the siderophore-negative mutant with regard to the control of fusarium wilt was related to the production of pseudobactin 358. The production of pseudobactin 358 appeared to be responsible for the increased suppression by Fo47b10 combined with WCS358 relative to that with Fo47b10 alone.     

Impact of a New Source of Resistance to Fusarium Wilt in Pigeonpea

Pigeonpea is an important grain legume grown by smallholder farmers in Southern Africa. Fusarium wilt, caused by the fungal pathogen Fusarium udum Butler, is the major disease limiting pigeonpea production in the region. This study was designed to evaluate the reaction to fusarium wilt as well as agronomic performance of new elite pigeonpea germplasm in three different countries during the 2001/2002 cropping season using wilt‐sick plots. Per cent incidence of fusarium wilt (%FW), grain size and yield, were measured. The genotype ICEAP 00040 consistently showed a high (<20.0%) level of resistance to the disease in all three countries. In contrast, %FW score for the susceptible genotype ICEAP 00068 was 87.5, 92.0 and 90.9% in Kenya, Malawi and Tanzania, respectively. The grain size obtained for ICEAP 00040 at Ngabu (Malawi) was 25.0% larger than that at each of the remaining locations indicating environmental influence on this trait. At all the three locations, ≥1.5 ton/Ha of grain yield was obtained for ICEAP 00040 compared with <1.0 ton/Ha for ICEAP 00068. In 2003, this improved resistant genotype (ICEAP 00040) was released for commercial production and will be useful as a good source of resistance in pigeonpea genetic improvement programs in the region.     

Suppression of bacterial wilt in Eucalyptus urophylla by fluorescent Pseudomonas spp. in China

Bacterial wilt caused by Ralstonia solanacearum race 1, biovar III has become a severe problem in Eucalyptus plantations in south China. The disease mainly attacks young eucalypt trees, and no effective control measures are available yet. To explore possibilities to develop biological control of the disease, strains of fluorescent Pseudomonas spp. that are effective in suppressing plant diseases by known mechanisms, were tested for their potential to control bacterial wilt in Eucalyptus. Pseudomonas putida WCS358r, Pseudomonas fluorescens WCS374r, P. fluorescens WCS417r, and Pseudomonas aeruginosa 7NSK2 antagonize R. solanacearum in vitro by siderophore-mediated competition for iron, whereas inhibition of pathogen growth by P. fluorescens CHA0r is antibiosis-based. No correlations were found between antagonistic activities of these Pseudomonas spp. in vitro and biocontrol of bacterial wilt in Eucalyptus in vivo. None of the strains suppressed disease when mixed together with the pathogen through the soil or when seeds or seedlings were treated with the strains one to four weeks before transfer into soil infested with R. solanacearum. However, when the seedlings were dipped with their roots in a bacterial suspension before transplanting into infested soil, P. fluorescens WCS417r significantly suppressed bacterial wilt. P. putida WCS358r was marginally effective, whereas its siderophore-minus mutant had no effect at all, indicating that siderophore-mediated competition for iron can contribute but is not effective enough to suppress bacterial wilt in Eucalyptus. A derivative of P. putida WCS358r, constitutively producing 2,4-diacetylphloroglucinol (WCS358::phl) reduced disease. Combined treatment with P. fluorescens WCS417r and P. putida WCS358::phl did not improve suppression of bacterial wilt.     

The effect of reduced phytoalexin production on the resistance of upland cotton (Gossypium hirsutum) to verticillium and fusarium wilts

The effect on disease development of inhibiting the production of the sesquiterpenoid phytoalexin hemigossypol (HG) in cotton resistant to both verticillium and fusarium wilts was investigated. Inhibition was achieved by treating the plants with the sodium salt of compactin, a competitive inhibitor of hydroxy-methylglutaryl (HMG) CoA reductase. Compactin treatment (150 μg litre^-1) reduced HG production by a mean of 48%. The enzyme inhibitor did not mimic symptoms in uninfected plants or significantly reduce the ability of the conidia of either Fusarium oxysporum f.sp. vasinfectum or Verticillium dahliae to germinate. Treatment of infected plants with compactin resulted in a breakdown of resistance to verticillium wilt but not to fusarium wilt. These results support the view that HG production is the primary mechanism of resistance to verticillium wilt, but not to fusarium wilt.     

The Effect of Temperature on Symptom Expression and Colonization in Resistant and Susceptible Carnation Cultivars Infected with Fusarium oxysporum f. sp. dianthi

Six commercial carnation cultivars were inoculated with Fusarium oxysporum f. sp. dianthi race 2, and grown under three different temperature regimes. Colonization by the pathogen and development of wilt symptoms were assessed at intervals up to 40 days. No symptoms and very little colonization were seen in any of the cultivars at 14–15°C. At a temperature of 22°C, the cultivars were clearly differentiated into three groups: those with resistance, partial resistance or susceptibility to the pathogen depending on the severity of symptoms and the extent of fungal colonization. Symptom severity was associated with the extent of colonization. This differentiation was not seen at 26°C, when all cultivars except the most resistant, cv.‘Carrier 929′, rapidly became diseased and died by 23 days after inoculation. ‘Carrier 929’ also showed some wilt symptoms at this temperature and was colonized throughout the height of the stem after 40 days. The pathogen caused disease at 26°C by a combination of vascular wilting and stem base and root rotting. Fungal colonization was assayed at 22°C by the dilution plate/homogenization method and by estimation of fungal chitin in a highly resistant (‘Carrier 929′) and in a highly susceptible (‘Red Baron’) cultivar. Both methods of assay gave similar results. In ‘Red Baron’, colonization increased slowly up to 20 days after inoculation then progressed rapidly, closely following the development of severe wilt symptoms. In ‘Carrier 929’, colonization remained very low. The low level of fungal biomass in ‘Carrier 929’ compared with ‘Red Baron’ indicated that the former cultivar showed true resistance as opposed to tolerance to the disease.     

长江流域棉区棉花新品种抗病虫性研究

2003年,对长江流域棉区15份新材料进行了抗红铃虫鉴定,结果有8份材料高抗红铃虫,占鉴定材料的53.33%;4份材料抗红铃虫,占26.67%;3份材料中抗红铃虫,占20.00%.对55份新材料进行抗枯萎病鉴定,结果有27份材料抗枯萎病,占鉴定材料的49.09%;26份材料耐枯萎病,占47.27%;2份感枯萎病,占3.64%.对59份材料进行抗黄萎病鉴定,结果有8份材料抗黄萎病,占鉴定材料的13.56%;43份材料耐黄萎病,占72.88%;8份材料感黄萎病,占13.56%.     

Biocontrol efficacy of Trichoderma asperellum MSST against tomato wilting by Fusarium oxysporum f. sp. lycopersici

Tomato is a popular vegetable widely grown in the tropics, which is mainly attacked by fusarium wilt incited by Fusarium oxysporum f. sp. lycopersici (FOL). In the present scenario, an ecofriendly alternative strategy such as use of fungi from rhizosphere is being explored to combat the phytopathogen invasion. This study was carried out to evaluate the efficacy of Trichoderma asperellum MSST to promote the growth and yield parameters of tomato S-22, a susceptible variety. This study was also undertaken to manage fusarium wilt disease under in vitro and in vivo conditions. Significant increase in vegetative parameters like root length, shoot length, plant weight and chlorophyll content 60 days after sowing (DAS) was observed. There was reduction in the incidence of fusarium wilt in tomato up to 85%. Increase in the level of total phenol, peroxidase, polyphenoloxidase and phenylalanine ammonium lyase activity at 10th day of pathogen inoculation showed enhancement of plant defence mechanism by T. asperellum MSST against FOL. Overall study revealed that isolate MSST was proven to be potential biocontrol agent showing induced resistance against FOL.     

Antagonistic Effect of Nonpathogenic Fusarium oxysporum Fo47 and Pseudobactin 358 upon Pathogenic Fusarium oxysporum f. sp. dianthi

Pseudobactin production by Pseudomonas putida WCS358 significantly improves biological control of fusarium wilt caused by nonpathogenic Fusarium oxysporum Fo47b10 (P. Lemanceau, P. A. H. M. Bakker, W. J. de Kogel, C. Alabouvette, and B. Schippers, Appl. Environ. Microbiol. 58:2978-2982, 1992). The antagonistic effect of Fo47b10 and purified pseudobactin 358 was studied by using an in vitro bioassay. This bioassay allows studies on interactions among nonpathogenic F. oxysporum Fo47b10, pathogenic F. oxysporum f. sp. dianthi WCS816, and purified pseudobactin 358, the fluorescent siderophore produced by P. putida WCS358. Both nonpathogenic and pathogenic F. oxysporum reduced each other's growth when grown together. However, in these coinoculation experiments, pathogenic F. oxysporum WCS816 was relatively more inhibited in its growth than nonpathogenic F. oxysporum Fo47b10. The antagonism of nonpathogenic F. oxysporum against pathogenic F. oxysporum strongly depends on the ratio of nonpathogenic to pathogenic F. oxysporum densities: the higher this ratio, the stronger the antagonism. This fungal antagonism appears to be mainly associated with the competition for glucose. Pseudobactin 358 reduced the growth of both F. oxysporum strains, whereas ferric pseudobactin 358 did not; antagonism by pseudobactin 358 was then related to competition for iron. However, the pathogenic F. oxysporum strain was more sensitive to this antagonism than the nonpathogenic strain. Pseudobactin 358 reduced the efficiency of glucose metabolism by the fungi. These results suggest that pseudobactin 358 increases the intensity of the antagonism of nonpathogenic F. oxysporum Fo47b10 against pathogenic F. oxysporum WCS816 by making WCS816 more sensitive to the glucose competition by Fo47b10.     

香蕉植株根区土壤的真菌多样性分析

尖孢镰孢菌古巴专化型(Fusarium oxysporum f.sp.cubense)是香蕉枯萎病的病原菌,该菌是一种土壤习居菌,了解香蕉根区土壤中真菌多样性及镰孢菌属(Fusarium)真菌所占比例,对如何减少土壤中的病原菌、预防香蕉枯萎病的发生有重要的指导意义。该文通过采集不同宿根年限的香蕉健康植株和枯萎病植株的根区土壤,利用高通量测序技术测定土壤样品中的真菌种群。结果表明:(1)同一宿根年限的香蕉植株中,健康植株根区土壤中所获的reads及OTUs数量均高于枯萎病植株,说明健康植株根区土壤的真菌多样性丰富于枯萎病植株。(2)除了一年生香蕉枯萎病植株以担子菌门(Basidiomycota)为主外,其他土壤样品中均以子囊菌门(Ascomycota)为主,其中的丛赤壳科最高相对丰度来自三年生健康植株的根区土壤(26.02%),其次是五年生的枯萎病植株根区土壤(15.56%)。(3)在丛赤壳科中,镰孢菌属在三年生健康植株土壤中的相对丰度最高(2.54%),在其他样品中的相对丰度在0.1%～0.65%之间;在镰孢菌属中,腐皮镰孢菌(Fusarium solani)的相对丰度(0～1.59%之间)高于尖孢镰孢菌(F.oxysporum),尖孢镰孢菌仅占很小的比例(相对丰度0～0.08%之间)。可见,在不同香蕉植株的根区土壤中,健康植株的根区土壤真菌多样性高于枯萎病植株,无论是健康植株还是枯萎病植株的根区土壤中,作为香蕉枯萎病病原菌的镰孢菌属或尖孢镰孢菌的群体均不占主导地位。     

Mutational analysis of genes determining antagonism of Alcaligenes sp. strain MFA1 against the phytopathogenic fungus Fusarium oxysporum.

Alcaligenes sp. strain MFA1 inhibits microconidial germination and germination-tube elongation of Fusarium oxysporum f.sp. dianthi and reduces the severity of fusarium wilt of carnation, presumably as a result of its production of a siderophore (G.Y. Yuen and M.N. Schroth. 1986. Phytopathology, 76:171-176). Derivative strains of MFA1, deficient in antagonism against F. oxysporum and in iron-limited growth, were obtained by Tn5 mutagenesis. The presence of a single Tn5 insertion in the genomic DNA of each derivative strain was detected by Southern analysis. Marker-exchange mutagenesis of strain MFA1 with DNA fragments, containing Tn5 and flanking sequences cloned from representative mutants, confirmed the association of single Tn5 insertions with the loss of antifungal activity and iron-independent growth of MFA1. These results are consistent with the involvement of siderophore biosynthesis by MFA1 in the inhibition of F. oxysporum.     

抗感枯萎病西瓜根际微生物比较研究

本文通过传统微生物培养方法,研究了在土培和基质培条件下,抗感枯萎病西瓜不同生育期根际和非根际微生物数量的变化.结果表明,微生物数量在根际显著高于在非根际微生物,且随西瓜生长发育的阶段不同而变化,苗期根际微生物数量最少,以后随西瓜生长发育,根际微生物数量不断增加,至生长旺盛的开花结果期,微生物数量达到最高,在西瓜生长发育后期,根际微生物数量又有所回落.西瓜抗枯萎病性与根际细菌的数量具有相关性,在生长发育各个阶段,无论是土培还是基质培,均表现为抗病材料的根际细菌数量高于感病材料的根际细菌数量.根际真菌与放线菌数量与西瓜的抗感枯萎病性没有相关性.非根际微生物数量在整个生育期变化辐度较小.非根际细菌数量在土培条件下几乎保持在同一水平,在基质培条件下迅速增加,至生长后期有所回落.非根际真菌与放线菌数量在土培和基质培条件下均于生长后期达到最高.     

Development of SRAP, SRAP-RGA, RAPD and SCAR markers linked with a Fusarium wilt resistance gene in eggplant

Fusarium wilt (Fusarium oxysporum Schlecht. f. sp. melongenae) is a vascular disease of eggplant (Solanum melongena L.). The objectives of this work were (1) to confirm the monogenic inheritance of fusarium wilt resistance in eggplant, (2) to identify molecular markers linked to this resistance, and (3) to develop SCAR markers from most informative markers. We report the tagging of the gene for resistance to fusarium wilt (FOM) in eggplant using SRAP, RGA, SRAP-RGA and RAPD markers. Analysis of segregation data confirmed the monogenic inheritance of resistance. DNA from F₂ and BC₁ populations of eggplant segregating for fusarium wilt resistance was screened with 2,316 primer combinations to detect polymorphism. Three markers were linked within 2.6 cM of the gene. The codominant SRAP marker Me8/Em5 and dominant SRAP-RGA marker Em12/GLPL2 were tightly linked to each other and mapped 1.2 cM from the resistance gene, whereas RAPD marker H12 mapped 2.6 cM from the gene and on the same side as the other two markers. The SRAP marker was converted into two dominant SCAR markers that were confirmed to be linked to the resistance gene in the F_2, BC₁ and F₂ of BC₃ generations of the same cross. These markers provide a starting point for mapping the eggplant FOM resistance gene in eggplant and for exploring the synteny between solanaceous crops for fusarium wilt resistance genes. The SCAR markers will be useful for identifying fusarium wilt-resistant genotypes in marker-assisted selection breeding programs using segregating progenies of the resistant eggplant progenitor used in this study.     

Developments of functional markers for <Emphasis Type="Italic">Fom</Emphasis>-<Emphasis Type="Italic">2</Emphasis>-mediated fusarium wilt resistance based on single nucleotide polymorphism in melon (<Emphasis Type="Italic">Cucumis melo</Emphasis> L.)

Three single nucleotide polymorphism (SNP) sites in which amino acids had changed were detected by sequence analysis within the leucine-rich repeat (LRR) region of the Fom-2 gene. Cleaved amplified polymorphic sequence (CAPS) and allele-specific PCR (AS-PCR) methods were employed to explore the SNP validation linked to fusarium wilt resistance in the F₁ and F₂ generations simultaneously. Homozygous- and heterozygous-resistant genotypes and homozygous-susceptible genotype could be clearly distinguished using the CAPS method, and three detected SNP sites were observed to be linked to fusarium wilt resistance, with a segregation ratio of 1:2:1 in the F₂ generation. In addition, heterozygous-resistant and homozygous-susceptible genotypes could be clearly distinguished in the F₁ generation using the AS-PCR method, showing a 3:1 segregation in terms of resistant and susceptible genotypes in the F₂ generation. We therefore developed SNP-based functional markers (FMs) and identified some melon germplasm resistant to fusarium wilt by FM analysis within melon species. In conclusion, the SNP-based FMs originating from the SNP site of the Fom-2 LRR region were determined to be linked to fusarium wilt resistance and showed promise in the enhancement of breeding in melon.     

甘薯兼抗薯瘟病和蔓割病种质筛选鉴定

用甘薯瘟2个致病型菌株对557份甘薯品种(系)分菌系做盆苗和田间接种鉴定,并用蔓割病菌接种鉴定.结果表明,筛选出兼抗薯瘟病2个菌系的品种(系)31份,兼抗甘薯瘟和蔓割病的品种(系)有16份,其中泉薯860、泉薯854、金山93、榕选416、金山908、广薯88-70和泉薯853等7份与我省主栽抗病品种湘薯75-55(CK)相比,具有类似的双抗性能力,而其抗瘟能力更强.福薯87、林泗2号、金山57和湛93-16等4份对照品种只抗单个病害或兼抗单个菌系.     

Interaction between Meloidogyne incognita and Fusarium oxysporum f. sp. phaseoli on Selected Bean Genotypes

Four bean genotypes (IPA-1, A-107, A-211, and Calima), representing all possible combinations of resistance and susceptibility to Fusarium oxysporum f. sp. phaseoli (Fop) and Meloidogyne incognita, were each inoculated with three population densities of these pathogens. Calima and A-107 were resistant to Fop; A-107 and A-211 were resistant to M. incognita; and IPA-1 was susceptible to both pathogens. In Fop-susceptible lines (IPA-1 and A-211), the presence of M. incognita contributed to an earlier onset and increased severity of Fusarium wilt symptoms and plant stunting. However, the Fop-resistant Calima developed symptoms of Fusarium wilt only in the presence of M. incognita. Genotype A-107 (resistant to both M. incognita and Fop) exhibited Fusarium wilt symptoms and a moderately susceptible reaction to Fop only after the breakdown of its M. incognita resistance by elevated incubation temperatures (27 C). Root galling and reproduction of M. incognita was generally increased as inoculum density of M. incognita was increased on the M. incognita susceptible cultivars. However, these factors were decreased as the inoculum density of Fop was increased. It was concluded that severe infections of bean roots by M. incognita increase the severity of Fusarium wilt on Fop-susceptible genotypes and may modify the resistant reaction to Fop.