Biological and molecular analyses of Beet necrotic yellow vein virus isolates that overcome host resistance genes

Author(s):  
Hsing-Yeh Liu ◽  
John L. Sears ◽  
Robert T. Lewellen
Plant Disease ◽  
2016 ◽  
Vol 100 (2) ◽  
pp. 380-387 ◽  
Author(s):  
Gerbert Sylvestre Dossa ◽  
Ricardo Oliva ◽  
Edgar Maiss ◽  
Casiana Vera Cruz ◽  
Kerstin Wydra

Rice bacterial blight (BB) is caused by Xanthomonas oryzae pv. oryzae and is responsible for substantial yield loss worldwide. Host resistance remains the most feasible control measure. However, pathogen variability leads to the failure of certain resistance genes to control the disease, and climate change with high amplitudes of heat predisposes the host plant to pathogen invasion. Due to pressure in natural selection, landrace species often carry a wide range of unique traits conferring tolerance of stress. Therefore, exploring their genetic background for host resistance could enable the identification of broad-spectrum resistance to combined abiotic and biotic stresses. Nineteen Oryza glaberrima accessions and O. sativa rice variety SUPA were evaluated for BB resistance under high temperature (35 and 31°C day and night, respectively) using 14 X. oryzae pv. oryzae strains originated from the Philippines. Under normal temperature, most of the accessions showed resistance to 9 strains (64.3%) and accession TOG6007 showed broad-spectrum resistance to 12 strains (85.7%). Under high temperature, most accessions showed a reduction in BB disease, whereas, accession TOG5620 showed disease reduction from all the X. oryzae pv. oryzae strains under high temperature. Molecular characterization using gene-based and linked markers for BB resistance genes Xa4, xa5, Xa7, xa13, and Xa21 revealed the susceptible alleles of Xa4, xa5, xa13, and Xa21 in O. glaberrima. However, no allele of Xa7 was detected among O. glaberrima accessions. Our results suggest that O. glaberrima accessions contain a BB resistance different from the Xa gene type. Genome-wide association mapping could be used to identify quantitative trait loci that are associated with BB resistance or combined BB resistance and high-temperature tolerance.


1985 ◽  
Vol 66 (7) ◽  
pp. 1553-1564 ◽  
Author(s):  
S. Bouzoubaa ◽  
H. Guilley ◽  
G. Jonard ◽  
K. Richards ◽  
C. Putz

2005 ◽  
Vol 6 (6) ◽  
pp. 615-627 ◽  
Author(s):  
YOSHIHIRO NARUSAKA ◽  
MARI NARUSAKA ◽  
MOTOAKI SEKI ◽  
JUNKO ISHIDA ◽  
KAZUO SHINOZAKI ◽  
...  

2015 ◽  
Vol 144 (2) ◽  
pp. 443-455 ◽  
Author(s):  
Nazli D. Kutluk Yilmaz ◽  
Miray Arli Sokmen ◽  
Riza Kaya ◽  
Mehmet Ali Sevik ◽  
Berna Tunali ◽  
...  

2016 ◽  
Vol 283 (1833) ◽  
pp. 20160778 ◽  
Author(s):  
Julien Martinez ◽  
Rodrigo Cogni ◽  
Chuan Cao ◽  
Sophie Smith ◽  
Christopher J. R. Illingworth ◽  
...  

Heritable symbionts that protect their hosts from pathogens have been described in a wide range of insect species. By reducing the incidence or severity of infection, these symbionts have the potential to reduce the strength of selection on genes in the insect genome that increase resistance. Therefore, the presence of such symbionts may slow down the evolution of resistance. Here we investigated this idea by exposing Drosophila melanogaster populations to infection with the pathogenic Drosophila C virus (DCV) in the presence or absence of Wolbachia , a heritable symbiont of arthropods that confers protection against viruses. After nine generations of selection, we found that resistance to DCV had increased in all populations. However, in the presence of Wolbachia the resistant allele of pastrel —a gene that has a major effect on resistance to DCV—was at a lower frequency than in the symbiont-free populations. This finding suggests that defensive symbionts have the potential to hamper the evolution of insect resistance genes, potentially leading to a state of evolutionary addiction where the genetically susceptible insect host mostly relies on its symbiont to fight pathogens.


Plant Disease ◽  
2019 ◽  
Vol 103 (8) ◽  
pp. 2083-2089 ◽  
Author(s):  
John J. Weiland ◽  
Kathrin Bornemann ◽  
Jonathan D. Neubauer ◽  
Mohamed F. R. Khan ◽  
Melvin D. Bolton

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania, a disease of global importance to the sugar beet industry. The most widely implemented resistance gene to rhizomania to date is Rz1, but resistance has been circumvented by resistance-breaking (RB) isolates worldwide. In an effort to gain greater understanding of the distribution of BNYVV and the nature of RB isolates in Minnesota and eastern North Dakota, sugar beet plants were grown in 594 soil samples obtained from production fields and subsequently were analyzed for the presence of BNYVV as well as coding variability in the viral P25 gene, the gene previously implicated in the RB pathotype. Baiting of virus from the soil with sugar beet varieties possessing no known resistance to rhizomania resulted in a disease incidence level of 10.6% in the region examined. Parallel baiting analysis of sugar beet genotypes possessing Rz1, the more recently introgressed Rz2, and with the combination of Rz1 + Rz2 resulted in a disease incidence level of 4.2, 1.0, and 0.8%, respectively. Virus sequences recovered from sugar beet bait plants possessing resistance genes Rz1 and/or Rz2 exhibited reduced genetic diversity in the P25 gene relative to those recovered from the susceptible genotype while confirming the hypervariable nature of the coding for amino acids (AAs) at position 67 and 68 in the P25 protein. In contrast to previous reports, we did not find an association between any one specific AA signature at these positions and the ability to circumvent Rz1-mediated resistance. The data document ongoing virulence development in BNYVV populations to previously resistant varieties and provide a baseline for the analysis of genetic change in the virus population that may accompany the implementation of new resistance genes to manage rhizomania.


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