scholarly journals Resistance Phenotypes in Diverse Accessions, Breeding Lines, and Cultivars of Three Mustard Species Inoculated with Turnip mosaic virus

Plant Disease ◽  
2010 ◽  
Vol 94 (11) ◽  
pp. 1290-1298 ◽  
Author(s):  
Monica A. Kehoe ◽  
Brenda A. Coutts ◽  
Roger A. C. Jones

The responses of 44 accessions, breeding lines, or cultivars of Brassica juncea (Indian mustard), 9 of B. carinata (Ethiopian mustard), 5 of B. nigra (black mustard), and 6 crosses between B. juncea and B. napus (canola) to sap inoculation with Turnip mosaic virus (TuMV) were investigated. Eleven different phenotypes were obtained, including six previously recognized in B. napus (+, O, R, RN, RN/+, and +N) and five not recorded before (+St, RN/St, RN/St/+, +N1, and +ND). All but two (+ and +St) were resistance phenotypes. The resistance phenotypes in B. carinata and B. juncea × B. napus crosses prevented systemic infection but those in B. juncea and B. nigra included systemic necrosis. Absence of systemic invasion associated with resistance phenotypes in B. carinata was confirmed by graft inoculations. The resistance phenotypes may reflect the presence of known TuMV resistance genes located in the A genome or unknown genes in the B genome in B. juncea, unknown resistance genes in the B or C genomes in B. carinata, and unknown resistance genes in the B genome in B. nigra. Further research to identify the resistance genes involved would establish the potential usefulness of these resistance phenotypes in breeding TuMV-resistant mustard cultivars for biofuel production.


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.



2019 ◽  
Vol 109 (9) ◽  
pp. 1638-1647
Author(s):  
Ik-Hyun Kim ◽  
Hye-Kyoung Ju ◽  
Junsu Gong ◽  
Jae-Yeong Han ◽  
Eun-Young Seo ◽  
...  

Infectious clones of Korean turnip mosaic virus (TuMV) isolates KIH1 and HJY1 share 88.1% genomic nucleotides and 96.4% polyprotein amino acid identity, and they induce systemic necrosis or mild mosaic, respectively, in Nicotiana benthamiana. Chimeric constructs between these isolates exchanged the 5′, central, and 3′ domains of KIH1 (K) and HJY1 (H), where the order of the letters indicates the origin of these domains. KIH1 and chimeras KHH and KKH induced systemic necrosis, whereas HJY1 and chimeras HHK, HKK, and HKH induced mild symptoms, indicating the determinant of necrosis to be within the 5′ 3.9 kb of KIH1; amino acid identities of the included P1, Helper component protease, P3, 6K1, and cylindrical inclusion N-terminal domain were 90.06, 98.91, 93.80, 100, and 100%, respectively. Expression of P1 or P3 from a potato virus X vector yielded symptom differences only between P3 of KIH1 and HJY1, implicating a role for P3 in necrosis in N. benthamiana. Chimera KKH infected Brassica rapa var. pekinensis ‘Norang’, which was resistant to both KIH1 and HJY1, indicating that two separate TuMV determinants are required to overcome the resistance. Ability of diverse TuMV isolates, chimeras, and recombinants to overcome resistance in breeding lines may allow identification of novel resistance genes.



2015 ◽  
Vol 31 (4) ◽  
pp. 363-370 ◽  
Author(s):  
Bong Nam Chung ◽  
Kyung San Choi ◽  
Jeong Joon Ahn ◽  
Jae Ho Joa ◽  
Ki Seck Do ◽  
...  


2019 ◽  
Vol 109 (5) ◽  
pp. 904-912 ◽  
Author(s):  
Junsu Gong ◽  
Hye-Kyoung Ju ◽  
Ik-Hyun Kim ◽  
Eun-Young Seo ◽  
In-Sook Cho ◽  
...  

Infectious clones were generated from 17 new Korean radish isolates of Turnip mosaic virus (TuMV). Phylogenetic analysis indicated that all new isolates, and three previously characterized Korean radish isolates, belong to the basal-BR group (indicating that the pathotype can infect both Brassica and Raphanus spp.). Pairwise analysis revealed genomic nucleotide and polyprotein amino acid identities of >87.9 and >95.7%, respectively. Five clones (HJY1, HJY2, KIH2, BE, and prior isolate R007) had lower sequence identities than other isolates and produced mild symptoms in Nicotiana benthamiana. These isolates formed three distinct sequence classes (HJY1/HJY2/R007, KIH2, and BE), and several differential amino acid residues (in P1, P3, 6K2, and VPg) were present only in mild isolates HJY1, HJY2, and R007. The remaining isolates all induced systemic necrosis in N. benthamiana. Four mild isolates formed a phylogenetic subclade separate from another subclade including all of the necrosis-inducing isolates plus mild isolate KIH2. Symptom severity in radish and Chinese cabbage genotypes was not correlated with pathogenicity in N. benthamiana; indeed, Chinese cabbage cultivar Norang was not infected by any isolate, whereas Chinese cabbage cultivar Chusarang was uniformly susceptible. Four isolates were unable to infect radish cultivar Iljin, but no specific amino acid residues were correlated with avirulence. These results may lead to the identification of new resistance genes against TuMV.



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 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.



2004 ◽  
Vol 85 (7) ◽  
pp. 2087-2098 ◽  
Author(s):  
Noriko Suehiro ◽  
Tomohide Natsuaki ◽  
Tomoko Watanabe ◽  
Seiichi Okuda

Turnip mosaic virus (TuMV, genus Potyvirus, family Potyviridae) infects mainly cruciferous plants. Isolates Tu-3 and Tu-2R1 of TuMV exhibit different infection phenotypes in cabbage (Brassica oleracea L.) and Japanese radish (Raphanus sativus L.). Infectious full-length cDNA clones, pTuC and pTuR1, were constructed from isolates Tu-3 and Tu-2R1, respectively. Progeny virus derived from infections with pTuC induced systemic chlorotic and ringspot symptoms in infected cabbage, but no systemic infection in radish. Virus derived from plants infected with pTuR1 induced a mild chlorotic mottle in cabbage and infected radish systemically to induce mosaic symptoms. By exchanging genome fragments between the two virus isolates, the P3-coding region was shown to be responsible for systemic infection by TuMV and the symptoms it induces in cabbage and radish. Moreover, exchanges of smaller parts of the P3 region resulted in recombinants that induced complex infection phenotypes, especially the combination of pTuC-derived N-terminal sequence and pTuR1-derived C-terminal sequence. Analysis by tissue immunoblotting of the inoculated leaves showed that the distributions of P3-chimeric viruses differed from those of the parents, and that the origin of the P3 components affected not only virus accumulation, but also long-distance movement. These results suggest that the P3 protein is an important factor in the infection cycle of TuMV and in determining the host range of this and perhaps other potyviruses.



2021 ◽  
Vol 12 ◽  
Author(s):  
Shiyou Qiu ◽  
Xuwei Chen ◽  
Yushan Zhai ◽  
Weijun Cui ◽  
Xuhong Ai ◽  
...  

The light-harvesting chlorophyll a/b complex protein 3 (LHCB3) of photosystem II plays important roles distributing the excitation energy and modulating the rate of state transition and stomatal response to abscisic acid. However, the functions of LHCB3 in plant immunity have not been well investigated. Here, we show that the expression of LHCB3 in Nicotiana benthamiana (NbLHCB3) was down-regulated by turnip mosaic virus (TuMV) infection. When NbLHCB3 was silenced by tobacco rattle virus-induced gene silencing, systemic infection of TuMV was inhibited. H2O2 was over-accumulated in NbLHCB3-silenced plants. Chemical treatment to inhibit or eliminate reactive oxygen species (ROS) impaired the resistance of the NbLHCB3-silenced plants to TuMV infection. Co-silencing of NbLHCB3 with genes involved in ROS production compromised the resistance of plants to TuMV but co-silencing of NbLHCB3 with genes in the ROS scavenging pathway increased resistance to the virus. Transgenic plants overexpressing NbLHCB3 were more susceptible to TuMV. These results indicate that downregulation of NbLHCB3 is involved in defense against TuMV by inducing ROS production.



Genome ◽  
2014 ◽  
Vol 57 (8) ◽  
pp. 419-425 ◽  
Author(s):  
Derek J. Lydiate ◽  
Rachel L. Rusholme Pilcher ◽  
Erin E. Higgins ◽  
John A. Walsh

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.



2010 ◽  
Vol 23 (2) ◽  
pp. 144-152 ◽  
Author(s):  
Bo Min Kim ◽  
Noriko Suehiro ◽  
Tomohide Natsuaki ◽  
Tsuyoshi Inukai ◽  
Chikara Masuta

Strains TuR1 and TuC of Turnip mosaic virus (TuMV) induce different symptoms on Arabidopsis thaliana ecotype Landsberg erecta (Ler); plants infected with TuR1 develop systemic necrosis, while TuC causes mosaics. We previously found that the Ler systemic necrosis was controlled by a single dominant gene, TuNI (TuMV necrosis inducer), and that it was actually a form of host defense response leading to a hypersensitive reaction (HR)-like cell death. To identify the viral factor interacting with TuNI, the domain swapping between the genomic clones of TuR1 and TuC was carried out, and we identified the TuMV symptom determinant interacting with TuNI as the P3 gene. Moreover, it was found that the central 0.5-kb domain of P3, including three different amino acids between the two isolates, was responsible for the systemic HR. To verify that the P3 gene can alone induce necrosis, we analyzed the constitutive P3 expression in Ler transgenic plants and the transient P3 expression in Ler protoplasts. These results indicated that P3 alone caused HR-like cell death. In this study, we successfully demonstrated that the systemic necrosis by TuMV in Arabidopsis was determined by the gene-for-gene interaction between TuNI and P3 using the protoplast system for direct verification.



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