Allelism Tests of Three Dominant Genes for Hypersensitive Resistance to Bacterial Spot of Pepper

1987 ◽  
Vol 77 (9) ◽  
pp. 1304 ◽  
Author(s):  
A. M. Hibberd
2009 ◽  
Vol 99 (9) ◽  
pp. 1037-1044 ◽  
Author(s):  
Matthew D. Robbins ◽  
Audrey Darrigues ◽  
Sung-Chur Sim ◽  
Mohammed Abu Taher Masud ◽  
David M. Francis

Bacterial spot of tomato is caused by four species of Xanthomonas. The accession PI 128216 (Solanum pimpinellifolium) displays a hypersensitive reaction (HR) to race T3 strains (predominately Xanthomonas perforans). We developed an inbred backcross (IBC) population (BC2S5, 178 families) derived from PI 128216 and OH88119 (S. lycopersicum) as the susceptible recurrent parent for simultaneous introgression and genetic analysis of the HR response. These IBC families were evaluated in the greenhouse for HR to race T3 strain Xcv761. The IBC population was genotyped with molecular markers distributed throughout the genome in order to identify candidate loci conferring resistance. We treated the IBC population as a hypothesis forming generation to guide validation in subsequent crosses. Nonparametric analysis identified an association between HR and markers clustered on chromosome 11 (P < 0.05 to 0.0001) and chromosome 6 (0.04 > P > 0.002). Further analysis of the IBC population suggested that markers on chromosome 6 and 11 failed to assort independently, a phenomenon known as gametic phase disequilibrium. Therefore, to validate marker-trait linkages, resistant IBC plants were crossed with OH88119 and BC3F2 progeny were evaluated for HR in the greenhouse. In these subsequent populations, the HR response was associated with the chromosome 11 markers (P < 0.0002) but not with the markers on chromosome 6 (P > 0.25). Independent F2 families were developed by crossing resistant IBC lines to OH8245, OH88119, and OH7530. These populations were genotyped, organized into classes based on chromosome 11 markers, and evaluated for resistance in the field. The PI 128216 locus on chromosome 11 provided resistance that was dependent on gene dosage and genetic background. These results define a single locus, Rx-4, from PI 128216, which provides resistance to bacterial spot race T3, has additive gene action, and is located on chromosome 11.


2011 ◽  
Vol 124 (3) ◽  
pp. 533-542 ◽  
Author(s):  
Chengcheng Pei ◽  
Hui Wang ◽  
Jieyun Zhang ◽  
Yuanyuan Wang ◽  
David M. Francis ◽  
...  

Plant Disease ◽  
2015 ◽  
Vol 99 (8) ◽  
pp. 1118-1124 ◽  
Author(s):  
Yanling Sun ◽  
Jingwei Zou ◽  
Huigai Sun ◽  
Wei Song ◽  
Xiaoming Wang ◽  
...  

Wheat powdery mildew (caused by Blumeria graminis f. sp. tritici) can be effectively managed by growing resistant cultivars. ‘Liangxing 66’ and ‘Wennong 14’ are the current winter wheat cultivars grown in northern China where powdery mildew is epidemic. Both cultivars have been demonstrated to carry single dominant genes for resistance to powdery mildew, tentatively designated PmLX66 and PmW14, on chromosome 5DS and share common linked markers with Pm2. Allelism tests were performed using a total of 15,657 plants of F2 segregating populations to determine the relationship between PmLX66, PmW14, and Pm2. All progeny from the crosses Liangxing 66 × ‘Ulka/8*Chancellor’ (Ulka/8*Cc), Wennong 14 × Ulka/8*Cc, and Liangxing 66 × Wennong 14 were resistant when tested with B. graminis f. sp. tritici isolate E20, indicating that PmLX66 and PmW14 are allelic to Pm2 and to each other. Liangxing 66 was resistant to 76.7% of the 60 B. graminis f. sp. tritici isolates from northern China, a slightly smaller proportion than Ulka/8*Cc (78.3%). However, Wennong 14 (85.0%) was more resistant against this set of B. graminis f. sp. tritici isolates than Ulka/8*Cc and Liangxing 66. Liangxing 66 and Wennong 14 differed from Ulka/8*Cc in respect to a number of B. graminis f. sp. tritici isolates. Based on these findings, PmLX66 and PmW14 are new alleles at the Pm2 locus.


Agronomy ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 26 ◽  
Author(s):  
Sadikshya Sharma ◽  
Krishna Bhattarai

Bacterial spot (BS), caused by four species of Xanthomonas: X. euvesicatoria, X. vesicatoria, X. perforans and X. gardneri in tomato (Solanum lycopersicum L.) results in severe loss in yield and quality by defoliation and the appearance of lesions on fruits, respectively. The combined industry standard for BS control (foliar applications Actigard® rotated with copper plus mancozeb) does not offer sufficient protection, especially when weather conditions favor disease spread. Development of tomato cultivars with BS resistance is thus an important measure to minimize losses. Hypersensitive and non-hypersensitive resistance has been identified in different wild accessions and cultivated tomato relatives and has been transferred to cultivated tomato. However, complete resistance is yet to be obtained. With the advent of next generation sequencing and precise genome editing tools, the genetic regions that confer resistance to bacterial spot can be targeted and enriched through gene pyramiding in a new commercial cultivar which may confer higher degree of horizontal resistance to multiple strains of Xanthomonas causing bacterial spot in tomato.


2007 ◽  
Vol 23 (3) ◽  
pp. 155-160 ◽  
Author(s):  
Byung-Soo Kim ◽  
Young-Chun Kim ◽  
Kwang-Sik Shin ◽  
Jeong-Hoon Kim

2011 ◽  
Vol 101 (10) ◽  
pp. 1217-1223 ◽  
Author(s):  
Hui Wang ◽  
Samuel F. Hutton ◽  
Matthew D. Robbins ◽  
Sung-Chur Sim ◽  
Jay W. Scott ◽  
...  

Bacterial spot of tomato (Solanum lycopersicum) is caused by four species of Xanthomonas. The disease causes significant yield losses and a reduction in fruit quality. Physiological races have been described with tomato race 3 (T3) corresponding to strains of Xanthomonas perforans. The breeding line Hawaii 7981 (hereafter H7981) shows a hypersensitive reaction (HR) to race T3 strains conditioned by the interaction of the host resistance locus Xv3 and the bacterial effector avrXv3. The Xv3 gene is required for H7981-derived resistance to be effective under field conditions, though its expression is subject to genetic background. The segregation of HR in F2 populations derived from H7981 crossed to processing tomato parents OH88119 and OH7870 was studied in 331 progeny, with the two independent crosses providing validation. We screened 453 simple-sequence repeat, insertion/deletion, and single-nucleotide polymorphism markers and identified 44 polymorphic markers each for the OH88119 and OH7870 populations covering 84.6 and 73.3% of the genome, respectively, within 20 centimorgans (cM). Marker–trait analysis using all polymorphic markers demonstrated that Xv3-mediated resistance maps to chromosome 11 in the two independent crosses. Allelism tests were conducted in crosses between lines carrying Xv3 derived from H7981, Rx-4 derived from plant introduction (PI) 128216, and resistance derived from PI 126932. These allelism tests suggested that the loci conditioning HR to race T3 strains are linked within 0.1 cM, are allelic, or are the same gene.


2002 ◽  
Vol 92 (3) ◽  
pp. 273-277 ◽  
Author(s):  
J. B. Jones ◽  
G. V. Minsavage ◽  
P. D. Roberts ◽  
R. R. Johnson ◽  
C. S. Kousik ◽  
...  

The pepper genotype, ECW-12346, was developed with bacterial spot resistance derived from Pep13, PI 271322, and ECW123 (Early Calwonder containing Bs1, Bs2, and Bs3 genes). For genetic analysis of this resistance, ECW12346, ECW123, F1, F2, and backcrosses were inoculated with a pepper race 6 (P6) strain. Two recessive genes were identified that determined resistance. The genes are designated bs5 and bs6 for the resistance derived from PI 271322 and Pep13, respectively. In greenhouse and field studies, ECW12346 was highly resistant, whereas ECW123 had significant defoliation. In growth-room studies, electrolyte leakage and population dynamics were determined. Following infiltration of both genotypes with 108 CFU/ml of a P6 strain, there was no rapid increase in electrolyte leakage within 72 h, whereas a rapid increase in electrolyte leakage occurred within 24 h when a similar concentration of a P3 strain (containing the avrBs2 gene) was infiltrated into the intercellular spaces of the leaf. When 105 CFU/ml of a P6 strain was infiltrated into leaves, complete tissue collapse was evident in ECW123 10 days later as determined by visual assessment and electrolyte leakage data, but no confluent necrosis was detected in ECW12346. Internal populations were at least two logarithmic units higher in ECW123 than in ECW12346. Therefore, ECW12346 inhibits population build-up without inducing the typical hypersensitive reaction characterized by an increase in electrolyte leakage.


2000 ◽  
Vol 13 (4) ◽  
pp. 402-412 ◽  
Author(s):  
Jaana H. Hämäläinen ◽  
Tuija Kekarainen ◽  
Christiane Gebhardt ◽  
Kazuo N. Watanabe ◽  
Jari P. T. Valkonen

Resistance to Potato virus A (PVA) was examined in a diploid cross involving Solanum tuberosum subsp. andigena as a resistance source. Hypersensitive resistance (HR) to PVA cosegregated with extreme resistance (ER) to Potato virus Y conferred by the dominant gene Ryadg on chromosome XI. Hence, HR to PVA was controlled by a novel, dominant resistance gene closely linked to Ryadg, or Ryadg recognized both viruses but conferred a different type of resistance to each virus. The HR prevented systemic infection with PVA following mechanical inoculation but not following graft inoculation. Another, recessive gene, ra, that may be linked or even allelic with Ryadg fully blocked vascular transport of PVA in graft-inoculated plants. Hence, a possibility exists that the genes for the three types of resistance to potyviruses may reside at the same, resistance gene-rich chromosome region syntenic in solanaceous species and might be related. The gene ra acted against all of the three PVA strains tested and, therefore, the avirulence determinants could not be mapped. However, also, PVA strain-specific resistance was found in the progeny. It was overcome by mutations introduced into the viral genome-linked protein and the helper component proteinase and/or the coat protein.


Crop Science ◽  
1988 ◽  
Vol 28 (1) ◽  
pp. 41-43 ◽  
Author(s):  
P. M. Hanson ◽  
C. D. Nickell ◽  
L. E. Gray ◽  
S. A. Sebastian

2015 ◽  
Vol 28 (6) ◽  
pp. 727-735 ◽  
Author(s):  
Andrew R. Russell ◽  
Tom Ashfield ◽  
Roger W. Innes

The Pseudomonas syringae effector AvrB triggers a hypersensitive resistance response in Arabidopsis and soybean plants expressing the disease resistance (R) proteins RPM1 and Rpg1b, respectively. In Arabidopsis, AvrB induces RPM1-interacting protein kinase (RIPK) to phosphorylate a disease regulator known as RIN4, which subsequently activates RPM1-mediated defenses. Here, we show that AvrPphB can suppress activation of RPM1 by AvrB and this suppression is correlated with the cleavage of RIPK by AvrPphB. Significantly, AvrPphB does not suppress activation of RPM1 by AvrRpm1, suggesting that RIPK is not required for AvrRpm1-induced modification of RIN4. This observation indicates that AvrB and AvrRpm1 recognition is mediated by different mechanisms in Arabidopsis, despite their recognition being determined by a single R protein. Moreover, AvrB recognition but not AvrRpm1 recognition is suppressed by AvrPphB in soybean, suggesting that AvrB recognition requires a similar molecular mechanism in soybean and Arabidopsis. In support of this, we found that phosphodeficient mutations in the soybean GmRIN4a and GmRIN4b proteins are sufficient to block Rpg1b-mediated hypersensitive response in transient assays in Nicotiana glutinosa. Taken together, our results indicate that AvrB and AvrPphB target a conserved defense signaling pathway in Arabidopsis and soybean that includes RIPK and RIN4.


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