Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially regulate symptom expression in Brassica rapa cultivars

Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially... In the pathosystem of Brassica rapa and turnip mosaic virus (TuMV), the type of symptoms expressed by susceptible plants are determined by the gene combinations between the host cultivar and virus strain. In this study, we found that the resistance reaction and symptoms such as systemic lethal necrosis, leaf malformation and mosaic were differentially determined, depending on the combinations of the genotypes for a host locus or two closely linked host loci and the viral CI gene. Systemic necrosis caused by TuMV-UK1 on some B. rapa subsp. pekinensis cultivars is induced in conjunction with a recessive gene, rnt1-2 ( r esistance and n ecrosis to t umv 1-2), which is allelic or closely linked to TuMV resistance gene Rnt1-1 on chromosome R6. rnt1-2 is incompletely recessive to rnt1-3 , which does not cause any necrotic responses. The genotype rnt1-2 / rnt1-3 caused a mild necrosis along leaf veins of severely malformed leaves. A spontaneous mutant, TuMV-UK1 (UK1m), with the amino acid substitution V1827E in CI, broke Rnt1-1 resistance and altered the systemic necrosis and leaf malformation induced by rnt1-2 . This single amino acid in the CI protein of UK1 was also associated with severe mosaic and abnormal leaf development, perhaps interacting with unknown host factors. To clarify the relationship between Rnt1-1 and TuRB01b , which was previously reported as a TuMV-UK1 resistance gene on chromosome R6, the B. rapa cultivar Tropical Delight carrying TuRB01b was inoculated with UK1m or the infectious UK1 clone with the CI V1827E mutation. Because Tropical Delight showed resistance to both mutants, Rnt1-1 might be different from TuRB01b . http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially regulate symptom expression in Brassica rapa cultivars

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Publisher
Springer Vienna
Copyright
Copyright © 2011 by Springer-Verlag
Subject
Biomedicine; Infectious Diseases; Medical Microbiology; Virology
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-011-1036-6
Publisher site
See Article on Publisher Site

Abstract

In the pathosystem of Brassica rapa and turnip mosaic virus (TuMV), the type of symptoms expressed by susceptible plants are determined by the gene combinations between the host cultivar and virus strain. In this study, we found that the resistance reaction and symptoms such as systemic lethal necrosis, leaf malformation and mosaic were differentially determined, depending on the combinations of the genotypes for a host locus or two closely linked host loci and the viral CI gene. Systemic necrosis caused by TuMV-UK1 on some B. rapa subsp. pekinensis cultivars is induced in conjunction with a recessive gene, rnt1-2 ( r esistance and n ecrosis to t umv 1-2), which is allelic or closely linked to TuMV resistance gene Rnt1-1 on chromosome R6. rnt1-2 is incompletely recessive to rnt1-3 , which does not cause any necrotic responses. The genotype rnt1-2 / rnt1-3 caused a mild necrosis along leaf veins of severely malformed leaves. A spontaneous mutant, TuMV-UK1 (UK1m), with the amino acid substitution V1827E in CI, broke Rnt1-1 resistance and altered the systemic necrosis and leaf malformation induced by rnt1-2 . This single amino acid in the CI protein of UK1 was also associated with severe mosaic and abnormal leaf development, perhaps interacting with unknown host factors. To clarify the relationship between Rnt1-1 and TuRB01b , which was previously reported as a TuMV-UK1 resistance gene on chromosome R6, the B. rapa cultivar Tropical Delight carrying TuRB01b was inoculated with UK1m or the infectious UK1 clone with the CI V1827E mutation. Because Tropical Delight showed resistance to both mutants, Rnt1-1 might be different from TuRB01b .

Journal

Archives of VirologySpringer Journals

Published: Sep 1, 2011

References

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