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 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 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.

Genetic mapping of Russian wheat aphid resistance genes Dn2 and Dn4 in wheat

Genome ◽  
1998 ◽  
Vol 41 (2) ◽  
pp. 303-306 ◽  
Author(s):  
Z -Q Ma ◽  
A Saidi ◽  
J S Quick ◽  
NLV Lapitan
Keyword(s):  
Triticum Aestivum ◽  
Restriction Fragment Length Polymorphism ◽  
Resistance Genes ◽  
Fragment Length Polymorphism ◽  
Triticum Aestivum L ◽  
Russian Wheat Aphid ◽  
Aphid Resistance ◽  
Rflp Markers ◽  
Marker Assisted Breeding ◽  
Restriction Fragment Length

To obtain markers for marker-assisted breeding of Russian wheat aphid resistance in wheat (Triticum aestivum L.), resistance genes Dn2 and Dn4 were mapped with restriction fragment length polymorphism (RFLP) markers, using populations derived from PI 62660 x 'Carson' and PI 372129 x 'Yuma'. PI 262660 and PI 372129 are the donor parents of Dn2 and Dn4, respectively. A locus detected by marker KsuA1 was linked to Dn2 at a distance of 9.8 cM on the long arm of chromosome 7D, and a locus detected by marker ABC156 was 11.6 cM away from Dn4 on the short arm of chromosome 1D.Key words: Russian wheat aphid, RFLP markers, Triticum aestivum.

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.

Physical mapping of restriction fragment length polymorphism (RFLP) markers in homoeologous groups 1 and 3 chromosomes of wheat by in situ hybridization

Genome ◽  
2001 ◽  
Vol 44 (3) ◽  
pp. 401-412 ◽  
Author(s):  
X -F. Ma ◽  
K Ross ◽  
J P Gustafson
Keyword(s):  
In Situ Hybridization ◽  
Restriction Fragment Length Polymorphism ◽  
Restriction Fragment ◽  
Physical Mapping ◽  
Length Polymorphism ◽  
Fragment Length ◽  
Fragment Length Polymorphism ◽  
Rflp Markers ◽  
Restriction Fragment Length

Using wheat ditelosomic lines and in situ hybridization of biotin-labelled DNA probes, 18 restriction fragment length polymorphism (RFLP) markers were physically located on homoeologous groups 1 and 3 chromosomes of wheat. Most of the markers hybridized to chromosome arms in a physical order concordant with the genetic maps. A majority of the markers studied were clustered in non-C-banded, distal euchromatic areas, indicating the presence of recombination hot spots and cold spots in those regions. However, on 1BS the markers were well dispersed, which could be due to the abundance of heterochromatin throughout the arm. An inversion between Xpsr653 and Xpsr953 was observed on 1AL. One new Xpsr688 locus, approximately 20–26% from the centromere, was found on 1AS and 1BS. The physical location of Xpsr170 on group 3 chromosomes probably represents an alternative to the loci on the genetic map. Finally, Xpsr313 was mapped to two physical loci on 1DL. Five markers were located to bins consistent with the deletion-based physical maps.Key words: wheat, physical mapping, in situ hybridization.

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.

Restriction Fragment Length Polymorphism Assessment of the Heterogeneous Nature of Maize Population GT-MAS:gk and Field Evaluation of Resistance to Aflatoxin Production by Aspergillus flavus

2002 ◽  
Vol 65 (1) ◽  
pp. 167-171 ◽  
Author(s):  
B. Z. GUO ◽  
A. BUTRON ◽  
H. LI ◽  
N. W. WIDSTROM ◽  
R. E. LYNCH
Keyword(s):  
Cluster Analysis ◽  
Restriction Fragment Length Polymorphism ◽  
Length Polymorphism ◽  
Fragment Length Polymorphism ◽  
Field Evaluation ◽  
Aflatoxin Production ◽  
Inbred Lines ◽  
Rflp Markers ◽  
Maize Population ◽  
Restriction Fragment Length

Aflatoxin, produced by Aspergillus flavus, is one of the most toxic and carcinogenic substances known and contaminates many agricultural commodities such as corn, peanuts, cottonseed, and tree nuts. The challenge to breeders/plant pathologists is to identify lines that have resistance to aflatoxin production. Maize population GT-MAS:gk has been identified and released as a germplasm with resistance to aflatoxin contamination. In the present study, we assessed genetic divergence in the GT-MAS:gk population using restriction fragment length polymorphism (RFLP) DNA markers to survey 11 selfed inbred lines and conducted field evaluations for the dissimilarities in aflatoxin production among these inbred lines in comparison with a sister population, GT-MAS:pw,nf. The 11 selfed inbred lines were assayed for DNA polymorphism using 113 RFLP markers in 10 linkage groups covering 1,518.2 centimorgans (cM; unit of gene or chromosome size). Considerable variation among the inbreds was detected with RFLP markers, of which 42 probe-enzyme combinations gave 102 polymorphic bands. Cluster analysis based on genetic similarities revealed associations and variations among the tested lines. Three polymorphic groups were distinguished by cluster analysis. Two years of field evaluation data showed that aflatoxin concentrations among the lines were significantly different in both years (P < 0.001). Maturity data were also different. Thus, this study demonstrates that the maize population GT-MAS:gk is heterogeneous and that individuals may be different in resistance to A. flavus infection and aflatoxin production. Therefore, the most resistant lines should be inbred to increase homogeneity, and resistance should be confirmed through progeny testing.

A molecular linkage map of tomato displaying chromosomal locations of resistance gene analogs based on a Lycopersicon esculentum × Lycopersicon hirsutum cross

Genome ◽  
2002 ◽  
Vol 45 (1) ◽  
pp. 133-146 ◽  
Author(s):  
L P Zhang ◽  
A Khan ◽  
D Niño-Liu ◽  
M R Foolad
Keyword(s):  
Disease Resistance ◽  
Restriction Fragment Length Polymorphism ◽  
Fragment Length Polymorphism ◽  
Rflp Markers ◽  
Resistance Gene Analogs ◽  
Lycopersicon Hirsutum ◽  
R Genes ◽  
Molecular Linkage Map ◽  
Tomato Diseases ◽  
Restriction Fragment Length

A molecular linkage map of tomato was constructed based on a BC1 population (N = 145) of a cross between Lycopersicon esculentum Mill. line NC84173 (maternal and recurrent parent) and Lycopersicon hirsutum Humb. and Bonpl. accession PI126445. NC84173 is an advanced breeding line that is resistant to several tomato diseases, not including early blight (EB) and late blight (LB). PI126445 is a self-incompatible accession that is resistant to many tomato diseases, including EB and LB. The map included 142 restriction fragment length polymorphism (RFLP) markers and 29 resistance gene analogs (RGAs). RGA loci were identified by PCR amplification of genomic DNA from the BC1 population, using ten pairs of degenerate oligonucleotide primers designed based on conserved leucine-rich repeat (LRR), nucleotide binding site (NBS), and serine (threonine) protein kinase (PtoKin) domains of known resistance genes (R genes). The PCR-amplified DNAs were separated by denaturing polyacrylamide gel electrophoresis (PAGE), which allowed separation of heterogeneous products and identification and mapping of individual RGA loci. The map spanned 1469 cM of the 12 tomato chromosomes with an average marker distance of 8.6 cM. The RGA loci were mapped to 9 of the 12 tomato chromosomes. Locations of some RGAs coincided with locations of several known tomato R genes or quantitative resistance loci (QRLs), including Cf-1, Cf-4, Cf-9, Cf-ECP2, rx-1, and Cm1.1 (chromosome 1); Tm-1 (chromosome 2); Asc (chrromosme 3); Pto, Fen, and Prf (chromosome 5); OI-1, Mi, Ty-1, Cm6.1, Cf-2, CF-5, Bw-5, and Bw-1 (chromosome 6); I-1, I-3, and Ph-1 (chromosome 7); Tm-2a and Fr1 (chromosome 9); and Lv (chromosome 12). These co-localizations indicate that the RGA loci were either linked to or part of the known R genes. Furthermore, similar to that for many R gene families, several RGA loci were found in clusters, suggesting their potential evolutionary relationship with R genes. Comparisons of the present map with other molecular linkage maps of tomato, including the high density L. esculentum × Lycopersicon pennellii map, indicated that the lengths of the maps and linear order of RFLP markers were in good agreement, though certain chromosomal regions were less consistent than others in terms of the frequency of recombination. The present map provides a basis for identification and mapping of genes and QTLs for disease resistance and other desirable traits in PI126445 and other L. hirsutum accessions, and will be useful for marker-assisted selection and map-based gene cloning in tomato.Key words: disease resistance, genetic marker, molecular map, quantitative trait locus (QTL), restriction fragment length polymorphism (RFLP), RGAs.

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.

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