scholarly journals Turnip mosaic virus determinants of virulence for Brassica napus resistance genes

2002 ◽  
Vol 38 (SI 1 - 6th Conf EFPP 2002) ◽  
pp. S155-S157
Author(s):  
C.E. Jenner ◽  
F. Sánchez ◽  
K. Tomimura ◽  
K. Ohshima ◽  
F. Ponz ◽  
...  

Dominant resistance genes identified in Brassica napus lines are effective against some, but not all, Turnip mosaic virus<br />(TuMV) isolates. An infectious clone of an isolate (UK 1) was used as the basis of chimeric virus constructions using<br />resistance-breaking mutants and other isolates to identify the virulence determinants for three dominant resistance genes.<br />For the resistance gene TuRB01, the presence of either of two mutations affecting the cylindrical inclusion (CI) protein<br />converted the avirulent UK 1 to a virulent isolate. Acquisition of such mutations had a slight cost to viral fitness in<br />plants lacking the resistance gene. A similar strategy is being used to identify the virulence determinants for two more<br />resistance genes present in another B. napus line.

2003 ◽  
Vol 107 (7) ◽  
pp. 1169-1173 ◽  
Author(s):  
S. L. Hughes ◽  
P. J. Hunter ◽  
A. G. Sharpe ◽  
M. J. Kearsey ◽  
D. J. Lydiate ◽  
...  

2003 ◽  
Vol 16 (9) ◽  
pp. 777-784 ◽  
Author(s):  
Carol E. Jenner ◽  
Xiaowu Wang ◽  
Kenta Tomimura ◽  
Kazusato Ohshima ◽  
Fernando Ponz ◽  
...  

Two isolates of the potyvirus Turnip mosaic virus (TuMV), UK 1 and CDN 1, differ both in their general symptoms on the susceptible propagation host Brassica juncea and in their ability to infect B. napus lines possessing a variety of dominant resistance genes. The isolate CDN 1 produces a more extreme mosaic in infected brassica leaves than UK 1 and is able to overcome the resistance genes TuRB01, TuRB04, and TuRB05. The resistance gene TuRB03, in the B. napus line 22S, is effective against CDN 1 but not UK 1. The nucleic acid sequences of the UK 1 and CDN 1 isolates were 90% identical. The C-terminal half of the P3 protein was identified as being responsible for the differences in symptoms in B. juncea. A single amino acid in the P3 protein was found to be the avirulence determinant for TuRB03. Previous work already has identified the P3 as an avirulence determinant for TuRB04. Our results increase the understanding of the basis of plant-virus recognition, show the importance of the potyviral P3 gene as a symptom determinant, and provide a role in planta for the poorly understood P3 protein in a normal infection cycle.


2007 ◽  
Vol 58 (1) ◽  
pp. 67 ◽  
Author(s):  
Brenda A. Coutts ◽  
John A. Walsh ◽  
Roger A. C. Jones

Forty-three Australian cultivars or breeding lines of Brassica napus (canola, oilseed rape) and 2 cultivars of Brassica juncea (mustard) were inoculated with infective sap containing isolate WA-Ap of Turnip mosaic virus (TuMV), which belongs to TuMV pathotype 8. The types of reactions obtained were: necrotic spots in inoculated leaves without systemic infection (RN), chlorotic blotches in inoculated leaves without systemic infection (R), and chlorotic blotches in inoculated leaves accompanied by systemic infection that consisted of either necrotic spots (+N) or chlorotic blotches (+). The RN and +N reactions are consistent with those expected in the presence of 4 strain-specific TuMV resistance genes TuRB01 (+N response), TuRB03 (+N response) and TuRB04 with TuRB05 (RN), with + indicating a susceptible response. However, which resistance gene corresponds to the R response is unclear. The RN (TuRB04 with TuRB05) type of response was the commonest. Only one genotype lacked any TuMV resistance, and segregation for more than one different type of resistance response occurred within 22 genotypes and some segregated for resistance and susceptibility. Some genotypes segregated for all 3 types of resistance response found. The reaction of 2 plants of cv. Rivette was atypical as they developed both necrotic spots in inoculated leaves and systemic chlorotic spots. Since breeding for TuMV resistance is not undertaken in Australia, these results indicate frequent but inadvertent crossing with parental lines carrying TuMV resistance. Widespread occurrence of TuMV resistance genes and the possibility that many Australian TuMV isolates may not be well adapted to B. napus may explain the low incidence of this virus found in Australian B. napus crops.


Virology ◽  
2002 ◽  
Vol 300 (1) ◽  
pp. 50-59 ◽  
Author(s):  
Carol E. Jenner ◽  
Kenta Tomimura ◽  
Kazusato Ohshima ◽  
Sara L. Hughes ◽  
John A. Walsh

2013 ◽  
Vol 127 (2) ◽  
pp. 509-519 ◽  
Author(s):  
Mina Jin ◽  
Soo-Seong Lee ◽  
Lin Ke ◽  
Jung Sun Kim ◽  
Mi-Suk Seo ◽  
...  

1999 ◽  
Vol 99 (7-8) ◽  
pp. 1149-1154 ◽  
Author(s):  
J. A. Walsh ◽  
A. G. Sharpe ◽  
C. E. Jenner ◽  
D. J. Lydiate

2008 ◽  
Vol 21 (7) ◽  
pp. 931-936 ◽  
Author(s):  
A. L. Eggenberger ◽  
M. R. Hajimorad ◽  
J. H. Hill

In soybean, Rsv1, a single dominant resistance gene, invokes extreme resistance (ER) against most Soybean mosaic virus (SMV) strains, including SMV-N, but not SMV-G7, which provokes a virulent lethal systemic hypersensitive response (LSHR). The elicitor functions of the two viruses provoking Rsv1-mediated ER and LSHR have been mapped to the N-terminal 271 amino acids of P3 from SMV-N and SMV-G7, respectively, which differ by nine residues between the two strains. To identify amino acids of P3 from SMV-N provoking Rsv1-mediated ER, the unique residues of SMV-G7 were substituted with those of SMV-N. Of the mutants tested on Rsv1-genotype soybean, only SMV-G7I788R and SMV-G7T948A lost virulence. However, substitution of amino acids of SMV-N, individually or in combination, with the reciprocal residues from SMV-G7 at these two positions failed to confer virulence to SMV-N. In the search for additional virulence determinants, a series of SMV-N chimeras was generated in which fragments within a region from near the middle of the helper-component proteinase (HC-Pro) cistron to the 5′ end of the cytoplasmic inclusion cistron, nucleotides 1,605 to 3,787, were replaced with those of SMV-G7. Only SMV-N-derived chimeras harboring the 3′ region of HC-Pro, at least from nucleotide 2,013, and the entire 5′ end of P3 (nucleotides 2,430 to 3,237) from SMV-G7 were virulent whereas reciprocal exchanges resulted in loss of SMV-G7 virulence. This region of HC-Pro differs by three amino acids between SMV-N and SMV-G7. Analyses of SMV-G7-derived HC-Pro site-directed mutants showed that only SMV-G7M683R lost virulence on Rsv1-genotype soybean; however, SMV-NR682M failed to gain virulence. Nevertheless, an SMV-N derived mutant with three concurrent substitutions, R682M+R787I+A947T, gained virulence. The data indicate that both P3 and HC-Pro are involved in virulence of SMV on Rsv1-genotype soybean.


2019 ◽  
Author(s):  
◽  
Leilane Karam Rodrigues

O turnip mosaic virus (TuMV) infecta espécies de diferentes famílias botânicas, sendo o único potyvírus capaz de infectar brássicas. Pode ser transmistido mecanicamente e de modo não persistente por mais de 80 espécies de afídeos. O TuMV é classificado em 12 patotipos, de acordo com reações em linhagens de Brassica napus que contêm (ou não) diferentes genes de resistência ao TuMV. Apesar de ser considerado o vírus mais importante que infecta brássicas no mundo, ainda há pouca informação sobre esse vírus na América do Sul. Com o objetivo de avançar no conhecimento da ocorrência, variabilidade genética e de aspectos biológicos e epidemiológicos do TuMV no Brasil, foram identificados e caracterizados 44 isolados de diferentes regiões produtoras de olerícolas. Cinco isolados tiveram seus genomas completamente sequenciados e, de acordo com análises filogenéticas da porção genômica correspondente à capa proteica, agruparam-se nos clados “World-B”, “Basal-B” e “BR”.


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