scholarly journals Novel Fusarium Wilt Resistance Genes Uncovered in the Wild Progenitors and Heirloom Cultivars of Strawberry

2021 ◽  
Author(s):  
Dominique D. A. Pincot ◽  
Mitchell J. Feldmann ◽  
Michael A. Hardigan ◽  
Mishi V. Vachev ◽  
Peter M. Henry ◽  
...  

Fusarium wilt, a soilborne disease caused by Fusarium oxysporum f. sp. fragariae, poses a significant threat to strawberry (Fragaria × ananassa) production in many parts of the world. This pathogen causes wilting, collapse, and death in susceptible genotypes. We previously identified a dominant gene (FW1) on chromosome 2B that confers resistance to race 1 of the pathogen and hypothesized that gene-for-gene resistance to Fusarium wilt was widespread in strawberry. To explore this, a genetically diverse collection of heirloom and modern cultivars and wild octoploid ecotypes were screened for resistance to Fusarium wilt races 1 and 2. Here we show that resistance to both races is widespread and that resistance to race 1 is mediated by dominant genes (FW1, FW2, FW3, FW4, and FW5) on three non-homoeologous chromosomes (1A, 2B, and 6B). The resistance proteins encoded by these genes are not yet known; however, plausible candidates were identified that encode pattern recognition receptor or other proteins known to mediate gene-for-gene resistance in plants. High-throughput genotyping assays for SNPs in linkage disequilibrium with FW1-FW5 were developed to facilitate marker-assisted selection and accelerate the development of race 1 resistant cultivars. This study laid the foundation for identifying the genes encoded by FW1-FW5, in addition to exploring the genetics of resistance to race 2 and other races of the pathogen, as a precaution to averting a Fusarium wilt pandemic.

HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 868E-869
Author(s):  
John W. Scott* ◽  
Hesham A. Agrama ◽  
John P. Jones

Tomato (Lycopersicon esculentum) line E427 has resistance genes to three races of Fusarium oxysporum f.sp. lycopersici derived from L. pennellii (L.pen) accession LA 716 and L. pimpinellifolium (L.pimp) accession PI 126915. E427 was crossed to susc. Bonny Best and F2 and backcross seed were obtained. Progeny were inoculated separately with Fusarium wilt races 1, 2, or 3. Lines with suspected recombination of resistance were selfed and re-inoculated until disease reactions were homozygous. Four lines were obtained with resistance to both races 2 and 3, but susceptible to race 1. These lines had the L.pen alleles at RFLP markers linked to I-3 on chromosome 7 and lacked L.pimp alleles linked to I and I-2 on chromosome 11. Complementation (F2) data indicated race 2 resistance on chromosome 7 was controlled by a single dominant gene. Three lines were resistant to race 2, but susceptible to races 1 and 3. These lines had L.pimp alleles at TG105 indicating the presence of I-2, and no L.pen alleles at markers linked to I-3. Three lines were resistant to race 1, but susceptible to races 2 and 3. All three had L.pimp alleles at TG523 confirming linkage to I on chromosome 11 and no L.pen alleles at markers tightly linked to I-3. However, one of the lines had L.pen alleles at CT113 on chromosome 7. This and F2 complementation data suggests the possible location of a race 1 resistant locus, I1. Two lines that were Fusarium wilt race 3 resistant and susceptible to race 1 had intermediate resistance to race 2. These two lines did not have the L. pennellii alleles at TG183, TG174, and CT43 near the I-3 locus indicating crossovers in this region reduced race 2 resistance.


2004 ◽  
Vol 129 (3) ◽  
pp. 394-400 ◽  
Author(s):  
J.W. Scott ◽  
H.A. Agrama ◽  
J.P. Jones

Tomato (Lycopersicon esculentum) line E427 has resistance genes to all three races of Fusarium oxysporum f.sp. lycopersici derived from L. pennellii accession LA 716 and L. pimpinellifolium accession PI 126915. To determine genes that confer resistance to specific races of fusarium wilt, line E427 was crossed to susceptible `Bonny Best' and then F2 and backcross (to `Bonny Best') seed were obtained. Self-pollinations resulted in 337 lines and progeny of each line was inoculated separately with fusarium wilt races 1, 2, or 3. Plants from lines whose segregation suggested recombination of resistance were self-pollinated and reinoculated until disease reactions were homozygous. Four lines were obtained with resistance to both races 2 and 3, but susceptible to race 1. These lines had the L. pennellii alleles at restriction fragment length polymorphism (RFLP) markers linked to I-3 on chromosome 7 and lacked L. pimpinellifolium alleles linked to I and I-2 on chromosome 11. Complementation (F2) data indicated race 2 resistance on chromosome 7 was controlled by a single dominant gene. Three lines were resistant to race 2, but susceptible to races 1 and 3. These lines had L. pimpinellifolium alleles at TG105 and flanking markers encompassing a 14.4 cM region indicating the presence of I-2, and no L. pennellii alleles at markers linked to I-3. Three lines were resistant to race 1, but susceptible to races 2 and 3. All three lines had L. pimpinellifolium alleles at TG523 confirming linkage to I on chromosome 11 and no L. pennellii alleles at markers tightly linked to I-3. However, one of the lines, 415, had L. pennellii alleles at CT113 on chromosome 7. This data along with F2 complementation data suggests the possible existence of a second race 1 resistant locus, I1, in this region. The four lines resistant to both races 2 and 3 were backcrossed again to `Bonny Best' and self-pollinated progeny from 174 plants were screened as described above. Two lines derived from different BC1S1 lines that were fusarium wilt race 3 resistant and susceptible to race 1 had intermediate resistance to race 2. These two lines did not have the L. pennellii alleles at TG183, TG174, and CT43 near the I-3 locus indicating crossovers in this region resulted in reduced race 2 resistance. Collectively, this is the first clear break in the fusarium wilt race 2 and race 1 resistance linkage on chromosome 11. It appears that the race 1 resistance derived from PI 126915 is controlled by the I gene. On chromosome 7, there was a break between the I-3 and I1 genes indicating I-3 does not confer race 1 resistance. The crossovers resulting in reduced resistance to race 2 could be within a complex I-3 locus or a tightly linked race 2 locus.


1999 ◽  
Vol 124 (1) ◽  
pp. 28-31 ◽  
Author(s):  
Kevin E. McPhee ◽  
Abebe Tullu ◽  
John M. Kraft ◽  
Fred J. Muehlbauer

Plant breeders must be aware of sources of resistance to pathogens that affect their crops. Fusarium wilt caused by Fusarium oxysporum Schl. f. sp. pisi Snyd. & Hans. is a fungal disease that affects peas and is important worldwide. Resistance to the different races of the pathogen has been identified in adapted germplasm and from specific accessions in the United States World Collection of peas (Pisum sativum L.). The goal of this study was to evaluate the resistance to fusarium wilt race 2 in the Pisum core collection. Of the 452 accessions screened, 62 (14%) were resistant. The resistant accessions included accessions from P.s. ssp. elatius that were collected from 24 different countries. The wide distribution of resistance around the world precludes the identification of any single country or region as a source of resistance. Of the 62 accessions resistant to race 2, 39 are also resistant to race 1 based on data obtained from GRIN. One of the wild progenitors, PI 344012, possessed resistance to races 1 and 2.


1962 ◽  
Vol 42 (1) ◽  
pp. 69-77 ◽  
Author(s):  
E. N. Larter ◽  
H. Enns

Four barley varieties, each immune to a Valki-attacking culture of loose smut (designated as race 2), were studied with respect to the inheritance of their resistance. Jet (C.I. 967) and Nigrinudum (C.I. 2222) were each found to possess two independent dominant genes determining resistance. Steudelli (C.I. 2266) proved to be immune to race 2 through the action of a single dominant gene, while resistance of Hillsa (C.I. 1604) was found to be conditioned by two complementary dominant genes. The absence of susceptible F3 families in crosses between Jet, Nigrinudum, and Steudelli indicated that these three varieties have in common a gene or genes for resistance to the race of smut used. The two complementary genes for resistance in Hillsa proved to be distinct from those of the other three varieties under study.The use of genetic analyses of disease resistance based upon classification of F3 families of the backcross to the resistant source is described and the merits of such a method are discussed.


Plant Disease ◽  
2014 ◽  
Vol 98 (10) ◽  
pp. 1326-1332 ◽  
Author(s):  
Anthony P. Keinath ◽  
Richard L. Hassell

Fusarium wilt of watermelon, caused by the soilborne fungal pathogen Fusarium oxysporum f. sp. niveum race 2, is a serious, widespread disease present in major watermelon-growing regions of the United States and other countries. ‘Fascination,’ a high yielding triploid resistant to race 1, is grown in southeastern states in fields that contain a mixture of races 1 and 2. There is some benefit to using cultivars with race 1 resistance in such fields, even though Fascination is susceptible to Fusarium wilt caused by race 2. Experiments in 2012 and 2013 were done in fields infested primarily with race 2 and a mixture of races 1 and 2, respectively. Fascination was grafted onto four rootstock cultivars: bottle gourd (Lagenaria siceraria) ‘Macis’ and ‘Emphasis’ and interspecific hybrid squash (Cucurbita maxima× C. moschata) ‘Strong Tosa’ and ‘Carnivor.’ Nongrafted and self-grafted Fascination were used as susceptible control treatments. In both experiments, mean incidence of plants with symptoms of Fusarium wilt was ≥52% in the susceptible control treatments and ≤6% on the grafted rootstocks. Disease incidence did not differ between rootstock species or cultivars. In both years, Fascination grafted onto Strong Tosa and Macis produced more marketable-sized fruit than the susceptible control treatments. Grafted Emphasis and Carnivor also produced more fruit than the control treatments in 2012. The cucurbit rootstocks suppressed Fusarium wilt caused by race 2 and increased marketable yield of triploid watermelon grown in infested soil.


Plant Disease ◽  
2014 ◽  
Vol 98 (2) ◽  
pp. 255-266 ◽  
Author(s):  
A. P. Keinath ◽  
R. L. Hassell

Grafting watermelon (Citrullus lanatus var. lanatus) onto rootstocks of interspecific hybrid squash (Cucurbita moschata × C. maxima), bottle gourd (Lagenaria siceraria), or citron (Citrullus lanatus var. citroides) has been used in Asia and Israel to mange Fusarium wilt of watermelon caused by Fusarium oxysporum f. sp. niveum. The objectives of this study were to determine the frequency of infection of six rootstocks by F. oxysporum f. sp. niveum races 1 and 2 and the field performance of grafted rootstocks in Charleston, SC. Grafted and nongrafted watermelon and rootstock plants were inoculated in the greenhouse with race 1, race 2, or water (the control treatment). With both races, the frequency of recovery of F. oxysporum from scion and rootstock portions of inoculated watermelon plants grafted onto ‘Ojakkyo’ citron was greater than from watermelon plants grafted onto ‘Shintosa Camel’ and ‘Strong Tosa’ interspecific hybrid squash, and from plants grafted onto ‘Emphasis’, ‘Macis’, and ‘WMXP 3945’ bottlegourd. For nongrafted plants inoculated with race 1, percent recovery also was greater from Ojakkyo than from interspecific hybrid squash and bottlegourd. For nongrafted plants inoculated with race 2, F. oxysporum was recovered from the base of ≥79% of all inoculated plants. More than two-thirds (15) of 21 isolates recovered from the tops or scions of inoculated plants were pathogenic on watermelon. In spring 2010 and 2011, the six rootstocks were grafted with seedless watermelon ‘Tri-X 313’, which is susceptible to both races, and transplanted in a field infested with races 1 and 2 of F. oxysporum f. sp. niveum. Disease incidence for nongrafted and self-grafted Tri-X 313 (the control treatments) and Tri-X 313 grafted onto Ojakkyo citron did not differ significantly. Grafted watermelon plants produced greater weights and numbers of fruit than plants of the two control treatments. Nonpathogenic isolates of F. oxysporum and isolates of F. oxysporum f. sp. niveum colonized interspecific hybrid squash, bottlegourd, and grafted watermelon. The rootstocks evaluated, however, restricted movement of F. oxysporum f. sp. niveum into the watermelon scion, suppressed wilt symptoms, and increased fruit yields in an infested field.


Plant Disease ◽  
2000 ◽  
Vol 84 (2) ◽  
pp. 199-199
Author(s):  
R. C. Ploetz ◽  
J. L. Haynes

Race 3 of Fusarium oxysporum f. sp. lycopersici, cause of Fusarium wilt of tomato, Lycopersicon esculentum, was first recognized in Florida in 1982 on the west coast (Hillsborough and Manatee counties) (2). Approximately 10 years later, race 3 was reported in northeastern production areas of the state (Gadsden County) (1) and was observed on the east coast (Ft. Pierce area) (D. O. Chellemi, personal communication). During the 1998 to 1999 season, mature plants of Sanibel, a commercial tomato cultivar with resistance to races 1 and 2, were observed with symptoms of Fusarium wilt at the University of Florida's Tropical Research and Education Center in Homestead. Approximately 20% of the plants were conspicuously wilted, chlorotic, and necrotic in all or unilateral portions of the canopy. Internal, vascular discoloration in affected plants extended far into the canopy, distinguishing the disease from Fusarium crown rot, caused by F. oxysporum f. sp. radicis-lycopersici. Pure colonies of fungi were isolated from surface-disinfested (10 s with 70% ethanol, 2 min with 10% bleach) stem segments on potato dextrose agar (PDA) amended with streptomycin (100 mg/liter), rifamycin (50 mg/liter), and a commercial miticide (Danitol 2EHC [4 drops/liter]). Isolates were identified as F. oxysporum due to their production of typical falcate macroconidia with foot-shaped basal cells, microconidia borne in false heads only on mono-phialides, and chlamydospores. In replicated (three) greenhouse trials, six single-spore isolates were used to root-dip inoculate (107 conidia per ml) seedlings of differential tomato cultivars (Bonnie Best, no resistance; Manapal, race 1 resistance; Walter, race 1 and race 2 resistance). All isolates were pathogenic on each of the differential cultivars, and one isolate, 2-1, caused severe damage on Walter (mean rating of 3.5 on a 1 to 5 scale). The results were repeated in a second trial with the most virulent isolate. In both trials, pure colonies of F. oxysporum were recovered from symptomatic seedlings. Southeastern Florida is the last major tomatoproduction area in Florida to be affected by race 3 of F. oxysporum f. sp. lycopersici. References: (1) D. O. Chellemi and H. A. Dankers. Plant Dis. 76:861, 1992. (2) R. B. Volin and J. P. Jones. Proc. Fla. State Hortic. Soc. 95:268, 1982.


HortScience ◽  
1999 ◽  
Vol 34 (3) ◽  
pp. 454E-454
Author(s):  
Leigh K. Hawkins ◽  
Fenny Dane ◽  
Thomas L. Kubisiak ◽  
Billy Rhodes

Fusarium wilt, caused by the soilborne fungus Fusarium oxysporum f.sp. niveum (FON), is a serious disease of the watermelon (Citrullus lanatus). Three races of this pathogen (races 0, 1, and 2) have been identified based on differential pathogenicity assays. Most commercially available cultivars are resistant to races 0 and 1. Inheritance for resistance to these races is thought to be controlled by a single dominant gene. No cultivars are resistant to race 2 and resistance is thought to be a quantitative trait. F2 lines derived from a cross between the Fusarium-resistant Citrullus lanatus PI296341, and the Fusarium-susceptible watermelon cultivar `New Hampshire Midget' were used to generate a RAPD-based map of the Citrullus genome. F2:3 families were assayed in the greenhouse for resistance to races 1 and 2. Those families that were either highly resistant or highly susceptible were used in identifying markers linked to Fusarium wilt resistance. A preliminary map of the Citrullus genome based on random amplified polymorphic DNA (RAPD) markers has been expanded with the inclusion of simple sequence repeats (SSRs), amplified fragment length polymorphisms (AFLPs), and isozymes.


Plant Disease ◽  
2018 ◽  
Vol 102 (9) ◽  
pp. 1820-1827 ◽  
Author(s):  
Anthony P. Keinath ◽  
Paula A. Agudelo

Interspecific hybrid squash (Cucurbita maxima × C. moschata ‘Strong Tosa’) and bottle gourd (Lagenaria siceraria ‘Macis’) rootstocks are resistant to Fusarium oxysporum f. sp. niveum but susceptible to Meloidogyne incognita (Southern root-knot nematode). Coinfection of Early Prolific Straightneck summer squash (C. pepo) with root-knot nematode and F. oxysporum f. sp. niveum has been reported to increase susceptibility to Fusarium wilt. The objectives of this study were to determine whether such an interaction occurred between M. incognita and F. oxysporum f. sp. niveum races 1 and 2 on Strong Tosa, Macis, and watermelon cultivars Fascination (resistant to race 1) and Tri-X 313 (susceptible to both races). Hosts were inoculated in a greenhouse with one of four pathogen treatments: F. oxysporum f. sp. niveum, M. incognita, both pathogens, or neither pathogen. Galling was present on ≥10% of the root systems of 90% of the plants inoculated with M. incognita. Bottle gourd had less galling than interspecific hybrid squash. Plants not inoculated with F. oxysporum f. sp. niveum did not wilt. Four weeks after inoculation, incidence and severity of Fusarium wilt and recovery of F. oxysporum did not differ for any hosts inoculated with F. oxysporum f. sp. niveum alone and F. oxysporum f. sp. niveum plus M. incognita (host–treatment interactions not significant). In general, Early Prolific Straightneck grouped with the F. oxysporum f. sp. niveum-resistant rootstocks when inoculated with F. oxysporum f. sp. niveum race 2 and with the susceptible watermelon when inoculated with race 1, regardless of inoculation with M. incognita. Recovery of F. oxysporum from stems of inoculated watermelon was greater than recovery from the other three hosts, regardless of nematode inoculation. In conclusion, our experiments do not support the hypothesis that resistance to F. oxysporum f. sp. niveum in cucurbit rootstocks or resistant watermelon cultivars would be compromised when M. incognita infects the roots.


2003 ◽  
Vol 83 (2) ◽  
pp. 377-379 ◽  
Author(s):  
S. Neumann and A. G. Xue

Reactions of the 117 field pea cultivars available in Canada were evaluated to the four common races (1, 2, 5, and 6) of Fusarium oxysporum Schl. f. sp. pisi (van Hall) Sny. and Hans, the causal agent of fusarium wilt, in growth chambers. Based on the visual assessment of foliar wilt symptoms, 49 cultivars were resistant to at least one of the four races, and the remaining 68 cultivars were susceptible to all four races. Of these resistant cultivars, Ascona and 44 other cultivars were resistant to race 1; Impala to race 2; Aladin to races 1 and 2; and Radley and Princess to races 2, 5, and 6. In an effort to standardize the methodology for screening field pea for resistance to the pathogen, other quantitative parameters including shoot length, vascular discoloration, and shoot and root dry weights were evaluated on selected cultivars. Correlation analysis revealed that foliar wilt symptoms and the reduction in shoot length were highly correlated (r = -0.90, P < 0.01). The result suggests that the reduction in shoot length could be used to supplement the visual severity rating for fusarium wilt in field pea. Key words: Field pea, Pisum sativum, fusarium wilt, Fusarium oxysporum f. sp. pisi, resistance


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