scholarly journals RFLP-based Analysis of Recombination Among Resistance Genes to Fusarium Wilt

HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 868E-869
Author(s):  
John W. Scott* ◽  
Hesham A. Agrama ◽  
John P. Jones
Keyword(s):  
Fusarium Wilt ◽  
Resistance Genes ◽  
Dominant Gene ◽  
Chromosome 7 ◽  
Rflp Markers ◽  
Single Dominant Gene ◽  
Chromosome 11 ◽  
Intermediate Resistance ◽  
Race 1 ◽  
Race 2

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.

scholarly journals RFLP-based Analysis of Recombination among Resistance Genes to Fusarium Wilt Races 1, 2, and 3 in Tomato

2004 ◽  
Vol 129 (3) ◽  
pp. 394-400 ◽  
Author(s):  
J.W. Scott ◽  
H.A. Agrama ◽  
J.P. Jones
Keyword(s):  
Fusarium Wilt ◽  
Resistance Genes ◽  
Fragment Length Polymorphism ◽  
Dominant Gene ◽  
Chromosome 7 ◽  
Rflp Markers ◽  
Chromosome 11 ◽  
Race 1 ◽  
Race 2 ◽  
Restriction Fragment Length

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.

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 ◽  
...  
Keyword(s):  
Fusarium Wilt ◽  
Dominant Gene ◽  
Soilborne Disease ◽  
Resistance Proteins ◽  
In The Wild ◽  
Race 1 ◽  
Race 2 ◽  
Wild Progenitors ◽  
Dominant Genes ◽  
Gene For Gene

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.

scholarly journals Resistance of 25 Melon Cultigens to Race 1 and Race 2 of Fusarium Wilt under Two Soil Fumigation Treatments

HortScience ◽  
1995 ◽  
Vol 30 (4) ◽  
pp. 821C-821
Author(s):  
Timothy J Ng ◽  
James G. Kantzes
Keyword(s):  
Fusarium Wilt ◽  
Cucumis Melo ◽  
Commercial Production ◽  
Soil Fumigation ◽  
Plastic Mulch ◽  
Methyl Isothiocyanate ◽  
Intermediate Resistance ◽  
Race 1 ◽  
Clear Plastic ◽  
Race 2

Twenty-five melon (Cucumis melo L.) cultigens were screened for resistance to fusarium wilt in a field infested with race 1 and race 2 of Fusarium oxysporum f.sp. melonis in 1993 and 1994. Plants were grown on clear plastic mulch using commercial production recommendations. The soil was fumigated with methyl isothiocyanate at a broadcast rate of 340 liters·ha–1 in 1993, and with dichloropropene at a broadcast rate of 136 liters·ha–1 in 1994. Resistance was determined by the percentage of plants surviving 8 weeks after transplanting. In general, highly resistant cultigens (>90% survival) and highly susceptible cultigens (<20% survival) performed consistently in the two experiments. However, differences in performance between the two years were noted for cultigens with intermediate resistance, and their performance may have contributed to the significant cultigen × year interaction in this study.

scholarly journals Toward Fine Mapping of the Tomato Yellow Leaf Curl Virus Resistance Gene Ty-2 on Chromosome 11 of Tomato

HortScience ◽  
2009 ◽  
Vol 44 (3) ◽  
pp. 614-618 ◽  
Author(s):  
Yuanfu Ji ◽  
John W. Scott ◽  
David J. Schuster
Keyword(s):  
Resistance Genes ◽  
Dominant Gene ◽  
Tomato Yellow Leaf ◽  
Resistance Locus ◽  
Yellow Leaf ◽  
Chromosome 11 ◽  
Race 2 ◽  
Molecular Marker Analysis ◽  
Leaf Curl Virus ◽  
Leaf Curl

The whitefly-transmitted Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomatoes grown in tropical and subtropical regions of the world. Several genes of different origins conferring resistance to TYLCV have been introgressed to the cultivated tomato (Solanum lycopersicum), including the single dominant gene, Ty-2, that originated from S. habrochiates and was previously mapped to a 19-cM region on the long arm of chromosome 11 delimited by restriction fragment length polymorphism markers TG36 and TG393. In the present study, we confirmed the dominant inheritance of the Ty-2 gene from TYLCV evaluation and molecular marker analysis of an F2 segregating population derived from a commercial hybrid that carries the Ty-2 gene. Evaluating recombinants recovered from the F2 progeny for TYLCV resistance localized the Ty-2 gene to a marker interval of 5.5 cM between C2_At1g07960 (82.5 cM) and C2_At4g32930 (88 cM). Additional recombinants were identified for the target region carrying the Ty-2 gene. TYLCV evaluation of the progeny from these recombinants further delimited the Ty-2 gene to a 4.5-cM interval between C2_At1g07960 (82.5 cM) and cLEN-11-F24 (87 cM). The smaller introgressions no longer include the fusarium wilt race 2 resistance locus (I-2), which should facilitate combining the two resistance genes in cis configuration. The polymerase chain reaction-based markers developed from the present study can be used to precisely monitor the introgression of the Ty-2 gene, thus offering the opportunity to pyramid TYLCV resistance genes from different sources as well as resistance genes for other pathogens into elite tomato cultivars.

scholarly journals Independent Resistant Reactions Expressed in Root and Tuber of Potato Breeding Lines with Introgressed Resistance to Meloidogyne chitwoodi

2009 ◽  
Vol 99 (9) ◽  
pp. 1085-1089 ◽  
Author(s):  
C. R. Brown ◽  
H. Mojtahedi ◽  
L.-H. Zhang ◽  
E. Riga
Keyword(s):  
Genetic Factors ◽  
Dominant Gene ◽  
Breeding Line ◽  
Single Dominant Gene ◽  
Solanum Bulbocastanum ◽  
Chromosome 11 ◽  
Meloidogyne Chitwoodi ◽  
Tuber Resistance ◽  
Advanced Backcross ◽  
Resistance Breaking

Resistance to Meloidogyne chitwoodi was introgressed from Solanum bulbocastanum into the cultivated gene pool of potato. A single dominant gene is responsible for resistance to race 1 reproduction on the root system. An additional form of resistance was discovered in certain advanced backcross clones. A BC5 clone, PA99N82-4, resisted invasion of tubers by available nematode juveniles whether supplied by weeds or challenged by several root resistance-breaking pathotypes. This tuber resistance is inherited as a single dominant gene and is linked to RMc1(blb). Because this gene has been mapped to chromosome 11, tuber resistance genetic factors are inferred to be on the same chromosome in coupling phase. Among 153 progeny derived from crosses with PA99N82-4, 42 recombinants, comprising both resistant root/susceptible tuber and susceptible root/resistant tubers, were found while other progeny were doubly resistant (like PA99N82-4) or doubly susceptible. Therefore, the existence of two linked genetic factors controlling independently expressed traits is confirmed. The combination of the two phenotypes is likely to be a sufficient level of resistance to avoid tuber damage from circumstances that provide exogenous juveniles proximal to the tubers in the soil. These factors are weed hosts of M. chitwoodi host races and pathotypes of M. chitwoodi that overcome RMc1(blb). Under field conditions, where a resistance-breaking pathotype of M. chitwoodi was present, tuber-resistant PA99N82-4 breeding line produced tubers which were commercially acceptable and not culled. A related breeding line, root resistant but tuber susceptible, and Russet Burbank were severely tuber damaged and commercially unacceptable.

scholarly journals Multiple Evolutionary Trajectories Have Led to the Emergence of Races in Fusarium oxysporum f. sp. lycopersici

2016 ◽  
Vol 83 (4) ◽  
Author(s):  
V. Chellappan Biju ◽  
Like Fokkens ◽  
Petra M. Houterman ◽  
Martijn Rep ◽  
Ben J. C. Cornelissen
Keyword(s):  
Transposable Elements ◽  
Fusarium Oxysporum ◽  
Resistance Genes ◽  
Pcr Analysis ◽  
Genomic Fragment ◽  
Avirulence Genes ◽  
Content Type ◽  
Race 1 ◽  
Tomato Cultivars ◽  
Race 2

ABSTRACT Race 1 isolates of Fusarium oxysporum f. sp. lycopersici (FOL) are characterized by the presence of AVR1 in their genomes. The product of this gene, Avr1, triggers resistance in tomato cultivars carrying resistance gene I. In FOL race 2 and race 3 isolates, AVR1 is absent, and hence they are virulent on tomato cultivars carrying I. In this study, we analyzed an approximately 100-kb genomic fragment containing the AVR1 locus of FOL race 1 isolate 004 (FOL004) and compared it to the sequenced genome of FOL race 2 isolate 4287 (FOL4287). A genomic fragment of 31 kb containing AVR1 was found to be missing in FOL4287. Further analysis suggests that race 2 evolved from race 1 by deletion of this 31-kb fragment due to a recombination event between two transposable elements bordering the fragment. A worldwide collection of 71 FOL isolates representing races 1, 2, and 3, all known vegetative compatibility groups (VCGs), and five continents was subjected to PCR analysis of the AVR1 locus, including the two bordering transposable elements. Based on phylogenetic analysis using the EF1-α gene, five evolutionary lineages for FOL that correlate well with VCGs were identified. More importantly, we show that FOL races evolved in a stepwise manner within each VCG by the loss of function of avirulence genes in a number of alternative ways. IMPORTANCE Plant-pathogenic microorganisms frequently mutate to overcome disease resistance genes that have been introduced in crops. For the fungus Fusarium oxysporum f. sp. lycopersici, the causal agent of Fusarium wilt in tomato, we have identified the nature of the mutations that have led to the overcoming of the I and I-2 resistance genes in all five known clonal lineages, which include a newly discovered lineage. Five different deletion events, at least several of which are caused by recombination between transposable elements, have led to loss of AVR1 and overcoming of I. Two new events affecting AVR2 that led to overcoming of I-2 have been identified. We propose a reconstruction of the evolution of races in FOL, in which the same mutations in AVR2 and AVR3 have occurred in different lineages and the FOL pathogenicity chromosome has been transferred to new lineages several times.

THE INHERITANCE OF LOOSE SMUT RESISTANCE.: I. THE INHERITANCE OF RESISTANCE IN FOUR BARLEY VARIETIES IMMUNE TO RACE 2 OF LOOSE SMUT

1962 ◽  
Vol 42 (1) ◽  
pp. 69-77 ◽  
Author(s):  
E. N. Larter ◽  
H. Enns
Keyword(s):  
Disease Resistance ◽  
Dominant Gene ◽  
The Other ◽  
Inheritance Of Resistance ◽  
Single Dominant Gene ◽  
Loose Smut ◽  
Race 2 ◽  
Or Genes ◽  
Dominant Genes

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.

IDENTIFICATION OF RESISTANCE GENES IN BARLEY BY REACTIONS TO USTILAGO NUDA

1969 ◽  
Vol 49 (4) ◽  
pp. 447-451 ◽  
Author(s):  
J. G. Moseman ◽  
D. R. Metcalfe
Keyword(s):  
Hordeum Vulgare ◽  
Resistance Genes ◽  
Smut Fungus ◽  
Loose Smut ◽  
Hordeum Vulgare L ◽  
Race 1 ◽  
Ustilago Nuda ◽  
Race 2 ◽  
Or Genes ◽  
Similar Gene

The reactions of 18 cultivars and selections of barley, Hordeum vulgare L., to inoculations with three cultures of the loose smut fungus, Ustilago nuda (Jens.) Rostr., were determined. The following conclusions were derived by analyzing the reactions of cultivars Jet (CI 967) and Milton (CI 4966) and derivatives from them to inoculations with cultures 244 of race 2, 49-70 of race 2, and 10 of race 1. Jet was shown to have two genes, Un3 and Un6, and Milton, one gene, Un8. Derivatives from Jet with only gene Un6 were distinguished from those with genes Un3 and Un6. Five host selections known to have a gene or genes at the same locus as Jet were shown to have gene Un6 or a similar gene at that locus.

scholarly journals Suppression of Fusarium Wilt Caused by Fusarium oxysporum f. sp. niveum Race 2 on Grafted Triploid Watermelon

Plant Disease ◽  
2014 ◽  
Vol 98 (10) ◽  
pp. 1326-1332 ◽  
Author(s):  
Anthony P. Keinath ◽  
Richard L. Hassell
Keyword(s):  
Fusarium Oxysporum ◽  
Fusarium Wilt ◽  
Disease Incidence ◽  
The United States ◽  
Infested Soil ◽  
Marketable Yield ◽  
Race 1 ◽  
Susceptible Control ◽  
Triploid Watermelon ◽  
Race 2

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.

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