The Sbm1 locus conferring resistance to Soil-borne cereal mosaic virus maps to a gene-rich region on 5DL in wheat

Genome ◽  
2006 ◽  
Vol 49 (9) ◽  
pp. 1140-1148 ◽  
Author(s):  
C. Bass ◽  
R. Hendley ◽  
M.J. Adams ◽  
K.E. Hammond-Kosack ◽  
K. Kanyuka
Keyword(s):  
Mosaic Virus ◽  
Resistance Gene ◽  
Cultural Practices ◽  
Mosaic Disease ◽  
Disease Resistance Gene ◽  
Resistance Locus ◽  
Rich Region ◽  
Resistant Cultivars ◽  
Germplasm Screening ◽  
Gene Rich Region

A mosaic disease caused by Soil-borne cereal mosaic virus (SBCMV) is becoming increasingly important, particularly in winter wheat in Europe. As there are currently no effective cultural practices or practical environmentally friendly chemicals for disease control, host plant resistance is an important objective in breeding programs. However, development of resistant cultivars is slow owing to difficulties in germplasm screening for resistance. Therefore, there is a need to identify molecular markers linked to SBCMV-resistance gene(s), so that quick and accurate laboratory-based marker-assisted selection rather than prolonged field-based screens for resistance can be used in developing resistant cultivars. We previously demonstrated that resistance to SBCMV in Triticum aestivum ‘Cadenza’ is controlled by a single locus. In this work, we used AFLP and microsatellite technology to map this resistance locus, with the proposed name Sbm1, to the distal end of chromosome 5DL. Interestingly, several expressed disease-resistance gene analogues also map to this gene-rich region on 5DL. Closely linked (~17 cM interval) markers, BARC110 and WMC765, RRES01 and BARC144, that flank Sbm1 will be very useful in breeding for selection of germplasm carrying Sbm1.

scholarly journals High-resolution mapping of Rym14Hb, a wild relative resistance gene to barley yellow mosaic disease

2020 ◽  
Author(s):  
Hélène Pidon ◽  
Neele Wendler ◽  
Antje Habekuβ ◽  
Anja Maasberg ◽  
Brigitte Ruge-Wehling ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Resistance Gene ◽  
Resistance Mechanism ◽  
Mosaic Disease ◽  
Yellow Mosaic Virus ◽  
Linkage Drag ◽  
Resistance Locus ◽  
Wild Relative ◽  
Yellow Mosaic Disease ◽  
Barley Breeding

Abstract Key message We mapped the Rym14Hb resistance locus to barley yellow mosaic disease in a 2Mbp interval. The co-segregating markers will be instrumental for marker-assisted selection in barley breeding. Abstract Barley yellow mosaic disease is caused by Barley yellow mosaic virus and Barley mild mosaic virus and leads to severe yield losses in barley (Hordeum vulgare) in Central Europe and East-Asia. Several resistance loci are used in barley breeding. However, cases of resistance-breaking viral strains are known, raising concerns about the durability of those genes. Rym14Hb is a dominant major resistance gene on chromosome 6HS, originating from barley’s secondary genepool wild relative Hordeum bulbosum. As such, the resistance mechanism may represent a case of non-host resistance, which could enhance its durability. A susceptible barley variety and a resistant H. bulbosum introgression line were crossed to produce a large F2 mapping population (n = 7500), to compensate for a ten-fold reduction in recombination rate compared to intraspecific barley crosses. After high-throughput genotyping, the Rym14Hb locus was assigned to a 2Mbp telomeric interval on chromosome 6HS. The co-segregating markers developed in this study can be used for marker-assisted introgression of this locus into barley elite germplasm with a minimum of linkage drag.

Map-based cloning of a gene sequence encoding a nucleotide-binding domain and a leucine-rich region at the Cre3 nematode resistance locus of wheat

Genome ◽  
1997 ◽  
Vol 40 (5) ◽  
pp. 659-665 ◽  
Author(s):  
Evans S. Lagudah ◽  
Odile Moullet ◽  
Rudi Appels
Keyword(s):  
Disease Resistance ◽  
Gene Family ◽  
Binding Site ◽  
Resistance Gene ◽  
Resistance Genes ◽  
Gene Sequence ◽  
Nucleotide Binding ◽  
Disease Resistance Gene ◽  
Leucine Rich Repeat ◽  
Rich Region

The Cre3 gene confers a high level of resistance to the root endoparasitic nematode Heterodera avenae in wheat. A DNA marker cosegregating with H. avenae resistance was used as an entry point for map-based cloning of a disease resistance gene family at the Cre3 locus. Two related gene sequences have been analysed at the Cre3 locus. One, identified as a cDNA clone, encodes a polypeptide with a nucleotide binding site (NBS) and a leucine-rich region; this member of the disease resistance gene family is expressed in roots. A second Cre3 gene sequence, cloned as genomic DNA, appears to be a pseudogene, with a frame shift caused by a deletion event. These two genes, related to members of the cytoplasmic NBS – leucine rich repeat class of plant disease resistance genes were physically mapped to the distal 0.06 fragment of the long arm of wheat chromosome 2D and cosegregated with nematode resistance.Key words: cereal cyst nematode, disease resistance genes, nucleotide-binding site, leucine-rich repeat.

Rps 8 Maps to a Resistance Gene Rich Region on Soybean Molecular Linkage Group F

Crop Science ◽  
2006 ◽  
Vol 46 (1) ◽  
pp. 168-173 ◽  
Author(s):  
Stuart G. Gordon ◽  
Steven K. St. Martin ◽  
Anne E. Dorrance
Keyword(s):  
Linkage Group ◽  
Resistance Gene ◽  
Rich Region ◽  
Molecular Linkage Group ◽  
Gene Rich Region

Identification of PCR-based markers flanking the recessive LMV resistance gene mo1 in an intraspecific cross in lettuce

Genome ◽  
1999 ◽  
Vol 42 (5) ◽  
pp. 982-986 ◽  
Author(s):  
S V Irwin ◽  
R V Kesseli ◽  
W Waycott ◽  
E J Ryder ◽  
J J Cho ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Resistance Gene ◽  
Bulked Segregant Analysis ◽  
Random Amplified Polymorphic Dna ◽  
Disease Resistance Gene ◽  
Symptom Development ◽  
Recessive Resistance ◽  
Lettuce Mosaic Virus ◽  
Recessive Resistance Gene ◽  
The Common

Molecular markers flanking the recessive resistance gene mo1 were identified following analysis of two segregating populations. Generation of a population from a crisphead × crisphead cross of Lactuca sativa that segregated for resistance conferred by the mo12 allele, but not morphological traits, was required for accurate mapping of the gene. Resistance was best assessed by symptom development after inoculating F3 families with the common pathotype II isolate of lettuce mosaic virus (LMV). Bulked segregant analysis for RAPD (random amplified polymorphic DNA) markers using one population, followed by linkage analysis using another, identified markers on either side of the mo1 gene, approximately 8 cM apart. These markers will be useful for more efficient introgression of this resistance gene into additional lettuce cultivars.Key words: lettuce, lettuce mosaic virus, molecular marker, disease resistance gene, bulked segregant analysis.

scholarly journals Two Novel DNAs That Enhance Symptoms and Overcome CMD2 Resistance to Cassava Mosaic Disease

2016 ◽  
Vol 90 (8) ◽  
pp. 4160-4173 ◽  
Author(s):  
Joseph Ndunguru ◽  
Leandro De León ◽  
Catherine D. Doyle ◽  
Peter Sseruwagi ◽  
German Plata ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Dna Sequences ◽  
Large Scale ◽  
Indian Subcontinent ◽  
Mosaic Disease ◽  
African Cassava Mosaic Virus ◽  
Cassava Mosaic Disease ◽  
Resistance Locus ◽  
East African ◽  
Cassava Mosaic Virus

ABSTRACTCassava mosaic begomoviruses (CMBs) cause cassava mosaic disease (CMD) across Africa and the Indian subcontinent. Like all members of the geminivirus family, CMBs have small, circular single-stranded DNA genomes. We report here the discovery of two novel DNA sequences, designated SEGS-1 and SEGS-2 (forsequencesenhancinggeminivirussymptoms), that enhance symptoms and break resistance to CMD. The SEGS are characterized by GC-rich regions and the absence of long open reading frames. Both SEGS enhanced CMD symptoms in cassava (Manihot esculentaCrantz) when coinoculated withAfrican cassava mosaic virus(ACMV),East African cassava mosaic Cameroon virus(EACMCV), orEast African cassava mosaic virus-Uganda(EACMV-UG). SEGS-1 also overcame resistance of a cassava landrace carrying the CMD2 resistance locus when coinoculated with EACMV-UG. Episomal forms of both SEGS were detected in CMB-infected cassava but not in healthy cassava. SEGS-2 episomes were also found in virions and whiteflies. SEGS-1 has no homology to geminiviruses or their associated satellites, but the cassava genome contains a sequence that is 99% identical to full-length SEGS-1. The cassava genome also includes three sequences with 84 to 89% identity to SEGS-2 that together encompass all of SEGS-2 except for a 52-bp region, which includes the episomal junction and a 26-bp sequence related to alphasatellite replication origins. These results suggest that SEGS-1 is derived from the cassava genome and facilitates CMB infection as an integrated copy and/or an episome, while SEGS-2 was originally from the cassava genome but now is encapsidated into virions and transmitted as an episome by whiteflies.IMPORTANCECassava is a major crop in the developing world, with its production in Africa being second only to maize. CMD is one of the most important diseases of cassava and a serious constraint to production across Africa. CMD2 is a major CMD resistance locus that has been deployed in many cassava cultivars through large-scale breeding programs. In recent years, severe, atypical CMD symptoms have been observed occasionally on resistant cultivars, some of which carry the CMD2 locus, in African fields. In this report, we identified and characterized two DNA sequences, SEGS-1 and SEGS-2, which produce similar symptoms when coinoculated with cassava mosaic begomoviruses onto a susceptible cultivar or a CMD2-resistant landrace. The ability of SEGS-1 to overcome CMD2 resistance and the transmission of SEGS-2 by whiteflies has major implications for the long-term durability of CMD2 resistance and underscore the need for alternative sources of resistance in cassava.

scholarly journals High-resolution mapping of Rym14Hb, a wild relative resistance gene to barley yellow mosaic disease

2020 ◽  
Author(s):  
Hélène Pidon ◽  
Neele Wendler ◽  
Antje Habekuβ ◽  
Anja Maasberg ◽  
Brigitte Ruge-Wehling ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Resistance Gene ◽  
Resistance Mechanism ◽  
Introgression Line ◽  
Mosaic Disease ◽  
Yellow Mosaic Virus ◽  
Linkage Drag ◽  
Wild Relative ◽  
Yellow Mosaic Disease ◽  
Fold Reduction

AbstractBarley yellow mosaic disease is caused by Barley yellow mosaic virus and Barley mild mosaic virus, and leads to severe yield losses in barley (Hordeum vulgare) in Central Europe and East-Asia. Several resistance loci are used in barley breeding. However, cases of resistance-breaking viral strains are known, raising concerns about the durability of those genes. Rym14Hb is a dominant major resistance gene on chromosome 6HS, originating from barley’s secondary genepool wild relative Hordeum bulbosum. As such, the resistance mechanism may represent a case of non-host resistance, which could enhance its durability. A susceptible barley variety and a resistant H. bulbosum introgression line were crossed to produce a large F2 mapping population (n=7,500), to compensate for a ten-fold reduction in recombination rate compared to intraspecific barley crosses. After high-throughput genotyping, the Rym14Hb locus was assigned to a 2Mbp telomeric interval on chromosome 6HS. The co-segregating markers developed in this study can be used for marker-assisted introgression of this locus into barley elite germplasm with a minimum of linkage drag.

Genetic control of immunity to Turnip mosaic virus (TuMV) pathotype 1 in Brassica rapa (Chinese cabbage)

Genome ◽  
2014 ◽  
Vol 57 (8) ◽  
pp. 419-425 ◽  
Author(s):  
Derek J. Lydiate ◽  
Rachel L. Rusholme Pilcher ◽  
Erin E. Higgins ◽  
John A. Walsh
Keyword(s):  
Mosaic Virus ◽  
Resistance Gene ◽  
Brassica Rapa ◽  
Chinese Cabbage ◽  
Turnip Mosaic Virus ◽  
Rflp Markers ◽  
Resistance Locus ◽  
Chromosome 6 ◽  
A Genome ◽  
Virus Interactions

Turnip mosaic virus (TuMV) is the major virus infecting crops of the genus Brassica worldwide. A dominant resistance gene, TuRB01b, that confers immunity to the virus isolate UK 1 (a representative pathotype 1 isolate of TuMV) on Brassica rapa was identified in the Chinese cabbage cultivar Tropical Delight. The TuRB01b locus was mapped to a 2.9-cM interval on B. rapa chromosome 6 (A6) that was flanked by RFLP markers pN101e1 and pW137e1. This mapping used a first backcross (B1) population segregating for the resistance gene at TuRB01b and sets of RFLP markers employed in previous mapping experiments in Brassica. Virus–plant interaction phenotypes were assayed in inbred progeny derived from B1 individuals to allow different virus isolates to be tested. Comparative mapping confirmed that A6 of B. rapa was equivalent to chromosome 6 of Brassica napus (A6) and that the map position of TuRB01b in B. rapa could be identical to that of TuRB01 in B. napus. Detailed evaluation of plant–virus interactions showed that TuRB01 and TuRB01b had indistinguishable specificities to a range of TuMV isolates. The possibility that TuRB01 and TuRB01b represent similar or identical alleles at the same A genome resistance locus suggests that B. napus acquired TuRB01 from the B. rapa gene pool.

scholarly journals Identification and Molecular Mapping of a Gummy Stem Blight Resistance Gene in Wild Watermelon (Citrullus amarus) Germplasm PI 189225

Plant Disease ◽  
2020 ◽  
Vol 104 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Runsheng Ren ◽  
Jinhua Xu ◽  
Man Zhang ◽  
Guang Liu ◽  
Xiefeng Yao ◽  
...  
Keyword(s):  
Resistance Gene ◽  
Molecular Mapping ◽  
Gene Annotation ◽  
Snp Markers ◽  
Chromosome 8 ◽  
Disease Resistance Gene ◽  
Resistance Locus ◽  
Annotation Database ◽  
Stem Blight ◽  
Gummy Stem Blight

Gummy stem blight (GSB), caused by Stagonosporopsis cucurbitacearum (syn. Didymella bryoniae), is a destructive foliar disease of watermelon in areas with hot and humid climates. The wild watermelon germplasm PI 189225 is a known source of resistance to GSB. The identification and use of molecular markers linked to resistance genes in the wild-type germplasm will speed up the introgression of GSB resistance into new watermelon varieties. An F2 segregating population was obtained from a cross between the resistant wild watermelon genotype PI 189225 and the susceptible genotype K3. The F2-derived F3 families were inoculated with a single isolate of S. cucurbitacearum (JS002) from Jiangsu Academy of Agricultural Sciences. The results of the genetic analysis demonstrated that GSB resistance in PI 189225 was controlled by a major quantitative trait locus (QTL), temporarily designated Qgsb8.1. Based on the results of bulk sergeant analysis and sequencing, one associated region spanning 5.7 Mb (10,358,659 to 16,101,517) on chromosome 8 was identified as responsible for the resistance to GSB using the Δ(single-nucleotide polymorphism [SNP]-index) method. The result of a QTL linkage analysis with Kompetitive allele-specific PCR (KASP) SNP markers further mapped the GSB resistance locus between the SNP markers KASP_JS9383 and KASP_JS9168 in a region of 571.27 kb on chromosome 8. According to the watermelon gene annotation database, the region contains approximately 19 annotated genes and, of these 19 genes, 2 are disease resistance gene analogs: Cla001017 (coiled-coil nucleotide-binding site leucine-rich repeat resistance protein) and Cla001019 (pathogenesis related). Reverse-transcription quantitative PCR demonstrated that the expression of the two genes changed following S. cucurbitacearum infection, suggesting that they play important roles in GSB resistance in watermelon. This result will facilitate fine mapping and cloning of the Qgsb8.1 locus, and the linked markers will further provide a useful tool for marker-assisted selection of this locus in watermelon breeding programs.

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