scholarly journals A series of eIF4E alleles at the Bc-3 locus are associated with recessive resistance to Clover yellow vein virus in common bean

2013 ◽  
Vol 126 (11) ◽  
pp. 2849-2863 ◽  
Author(s):  
John P. Hart ◽  
Phillip D. Griffiths
Keyword(s):  
Common Bean ◽  
Yellow Vein ◽  
Recessive Resistance ◽  
Clover Yellow Vein Virus

scholarly journals P3N-PIPO, a Frameshift Product from theP3Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

2016 ◽  
Vol 90 (16) ◽  
pp. 7388-7404 ◽  
Author(s):  
Go Atsumi ◽  
Haruka Suzuki ◽  
Yuri Miyashita ◽  
Sun Hee Choi ◽  
Yusuke Hisa ◽  
...  
Keyword(s):  
Cell Death ◽  
Resistance Gene ◽  
Systemic Infection ◽  
Viral Disease ◽  
Hypersensitive Reaction ◽  
Yellow Vein ◽  
Recessive Resistance ◽  
Content Type ◽  
Clover Yellow Vein Virus ◽  
And Control

ABSTRACTPeas carrying thecyv1recessive resistance gene are resistant to clover yellow vein virus (ClYVV) isolates No.30 (Cl-No.30) and 90-1 (Cl-90-1) but can be infected by a derivative of Cl-90-1 (Cl-90-1 Br2). The main determinant for the breaking ofcyv1resistance by Cl-90-1 Br2 is P3N-PIPO produced from theP3gene via transcriptional slippage, and the higher level of P3N-PIPO produced by Cl-90-1 Br2 than by Cl-No.30 contributes to the breaking of resistance. Here we show that P3N-PIPO is also a major virulence determinant in susceptible peas that possess another resistance gene,Cyn1, which does not inhibit systemic infection with ClYVV but causes hypersensitive reaction-like lethal systemic cell death. We previously assumed that the susceptible pea cultivar PI 226564 has a weak allele ofCyn1. Cl-No.30 did not induce cell death, but Cl-90-1 Br2 killed the plants. Our results suggest that P3N-PIPO is recognized byCyn1and induces cell death. Unexpectedly, heterologously strongly expressed P3N-PIPO of Cl-No.30 appears to be recognized byCyn1in PI 226564. The level of P3N-PIPO accumulation from theP3gene of Cl-No.30 was significantly lower than that of Cl-90-1 Br2 in aNicotiana benthamianatransient assay. Therefore,Cyn1-mediated cell death also appears to be determined by the level of P3N-PIPO. The more efficiently a ClYVV isolate brokecyv1resistance, the more it induced cell death systemically (resulting in a loss of the environment for virus accumulation) in susceptible peas carryingCyn1, suggesting that antagonistic pleiotropy of P3N-PIPO controls the resistance breaking of ClYVV.IMPORTANCEControl of plant viral disease has relied on the use of resistant cultivars; however, emerging mutant viruses have broken many types of resistance. Recently, we revealed that Cl-90-1 Br2 breaks the recessive resistance conferred bycyv1, mainly by accumulating a higher level of P3N-PIPO than that of the nonbreaking isolate Cl-No.30. Here we show that a susceptible pea line recognized the increased amount of P3N-PIPO produced by Cl-90-1 Br2 and activated the salicylic acid-mediated defense pathway, inducing lethal systemic cell death. We found a gradation of virulence among ClYVV isolates in acyv1-carrying pea line and two susceptible pea lines. This study suggests a trade-off between breaking of recessive resistance (cyv1) and host viability; the latter is presumably regulated by the dominantCyn1gene, which may impose evolutionary constraints uponP3N-PIPOfor overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.

scholarly journals Involvement of the P1 Cistron in Overcoming eIF4E-Mediated Recessive Resistance Against Clover yellow vein virus in Pea

2010 ◽  
Vol 23 (11) ◽  
pp. 1460-1469 ◽  
Author(s):  
Kenji S. Nakahara ◽  
Ryoko Shimada ◽  
Sun-Hee Choi ◽  
Haruko Yamamoto ◽  
Jun Shao ◽  
...  
Keyword(s):  
Systemic Infection ◽  
Translation Initiation Factor ◽  
Yellow Vein ◽  
Initiation Factor ◽  
Recessive Resistance ◽  
Nonsynonymous Mutation ◽  
Eukaryotic Translation ◽  
Clover Yellow Vein Virus ◽  
Recessive Genes ◽  
Eukaryotic Translation Initiation

Two recessive genes (cyv1 and cyv2) are known to confer resistance against Clover yellow vein virus (ClYVV) in pea. cyv2 has recently been revealed to encode eukaryotic translation initiation factor 4E (eIF4E) and is the same allele as sbm1 and wlm against other potyviruses. Although mechanical inoculation with crude sap is rarely able to cause infection of a cyv2 pea, biolistic inoculation of the infectious ClYVV cDNA clone does. At the infection foci, the breaking virus frequently emerges, resulting in systemic infection. Here, a derived cleaved-amplified polymorphic sequence analysis showed that the breakings were associated with a single nonsynonymous mutation on the ClYVV genome, corresponding to an amino-acid substitution at position 24 (isoleucine to valine) on the P1 cistron. ClYVV with the point mutation was able to break the resistance. This is a first report demonstrating that P1 is involved in eIF4E-mediated recessive resistance.

Resistance to Clover yellow vein virus in Common Bean Germplasm

Crop Science ◽  
2014 ◽  
Vol 54 (6) ◽  
pp. 2609-2618 ◽  
Author(s):  
John P. Hart ◽  
Phillip D. Griffiths
Keyword(s):  
Common Bean ◽  
Yellow Vein ◽  
Clover Yellow Vein Virus

scholarly journals Outbreak of Clover yellow vein virus in a Bean Field in Colusa County, California

Plant Disease ◽  
2001 ◽  
Vol 85 (4) ◽  
pp. 444-444 ◽  
Author(s):  
R. Crnov ◽  
R. L. Gilbertson
Keyword(s):  
Common Bean ◽  
Virus Disease ◽  
Sodium Dodecyl ◽  
Yellow Vein ◽  
Enzyme Linked Immunosorbent Assay ◽  
Rt Pcr ◽  
Systemic Necrosis ◽  
First Report ◽  
Bean Plants ◽  
Clover Yellow Vein Virus

In 1999, a severe outbreak (i.e., 100% infection) of a virus disease was observed in a single field of common bean in Colusa County, CA. The symptoms included a yellow mosaic, leaf epinasty and, in some plants, a systemic necrosis. This field was adjacent to a clover field that had been harvested early in the development of the bean plants. A preliminary serological test (enzyme-linked immunosorbent assay, ELISA) suggested that the virus infecting these bean plants was Peanut mottle virus (PeMoV). This would represent the first report of this virus in California. A range of common bean cultivars (Black Turtle Soup, Topcrop, California Early Light Red Kidney, and Sutter Pink) were inoculated with sap prepared from symptomatic leaves collected from this field. Symptoms developing on these plants ranged from systemic necrosis (cvs. Sutter Pink and Black Turtle Soup) to strong yellow green mosaic and leaf distortion (cvs. Topcrop and California Early Light Red Kidney). Furthermore, inoculated primary leaves of cv. Topcrop failed to develop local lesions, which is characteristic of PeMoV. ELISAs on all symptomatic plants with antisera against PeMoV, BYMV, BCMV, and BCMNV as well as reverse transcription polymerase chain reaction (RT-PCR) analysis with primer pairs specific for PeMoV, BYMV, BCMV, and BCMNV were negative. To further investigate the nature of this virus, a minipurification method was used to purify virions from symptomatic leaves of all four cultivars. Sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis of purified virions from these cultivars revealed a 32-kDa band consistent with infection by a potyvirus. Transmission electron microscopy analysis of these preparations revealed the presence of potyvirus-like flexous rods (approximately 750 nm long and 10 nm wide). We next designed a primer pair specific for the coat protein gene of Clover yellow vein virus (ClYVV) and RT-PCR with these primers resulted in the amplification of a 630-bp DNA fragment from four isolates of the unknown potyvirus. No fragments were amplified from an uninfected control. The PCR-amplified fragments were direct-sequenced, and sequence comparisons revealed that the sequences of all four isolates were 95% identical to that of ClYVV (Genbank accession number D89541). Subsequently, a ClYVV antiserum was obtained from Simon Scott (Department of Plant Pathology, Clemson University), and ELISAs performed on leaves infected with all four isolates were positive. Finally, to assess whether the virus was seed-transmitted, seed harvested from this field was planted in a greenhouse (two lots of 400 seed each). None of the plants from these seeds developed virus symptoms, suggesting that the virus was not seed-transmitted. Together, these results indicate that the virus disease outbreak in this bean field was caused by ClYVV rather than PeMoV. The inoculum source for the virus was probably the adjacent clover field. This is the first report of ClYVV infecting common bean in California.

scholarly journals Quantitative and Qualitative Involvement of P3N-PIPO in Overcoming Recessive Resistance against Clover Yellow Vein Virus in Pea Carrying the cyv1 Gene

2013 ◽  
Vol 87 (13) ◽  
pp. 7326-7337 ◽  
Author(s):  
S. H. Choi ◽  
Y. Hagiwara-Komoda ◽  
K. S. Nakahara ◽  
G. Atsumi ◽  
R. Shimada ◽  
...  
Keyword(s):  
Yellow Vein ◽  
Recessive Resistance ◽  
Clover Yellow Vein Virus

scholarly journals Recessive Resistance to Bean common mosaic virus Conferred by the bc-1 and bc-2 Genes in Common Bean (Phaseolus vulgaris) Affects Long-Distance Movement of the Virus

2018 ◽  
Vol 108 (8) ◽  
pp. 1011-1018 ◽  
Author(s):  
Xue Feng ◽  
Gardenia E. Orellana ◽  
James R. Myers ◽  
Alexander V. Karasev
Keyword(s):  
Phaseolus Vulgaris ◽  
Common Bean ◽  
Mosaic Virus ◽  
Bean Common Mosaic Virus ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Recessive Resistance ◽  
Long Distance ◽  
Systemic Spread ◽  
Long Distance Movement

Recessive resistance to Bean common mosaic virus (BCMV) in common bean (Phaseolus vulgaris) is governed by four genes that include one strain-nonspecific helper gene bc-u, and three strain-specific genes bc-1, bc-2, and bc-3. The bc-3 gene was identified as an eIF4E translation initiation factor gene mediating resistance through disruption of the interaction between this protein and the VPg protein of the virus. The mode of action of bc-1 and bc-2 in expression of BCMV resistance is unknown, although bc-1 gene was found to affect systemic spread of a related potyvirus, Bean common mosaic necrosis virus. To investigate the possible role of both bc-1 and bc-2 genes in replication, cell-to-cell, and long-distance movement of BCMV in P. vulgaris, we tested virus spread of eight BCMV isolates representing pathogroups I, IV, VI, VII, and VIII in a set of bean differentials expressing different combinations of six resistance alleles including bc-u, bc-1, bc-12, bc-2, bc-22, and bc-3. All studied BCMV isolates were able to replicate and spread in inoculated leaves of bean cultivars harboring bc-u, bc-1, bc-12, bc-2, and bc-22 alleles and their combinations, while no BCMV replication was found in inoculated leaves of cultivar IVT7214 carrying the bc-u, bc-2, and bc-3 genes, except for isolate 1755a, which was capable of overcoming the resistance conferred by bc-2 and bc-3. In contrast, the systemic spread of all BCMV isolates from pathogroups I, IV, VI, VII, and VIII was impaired in common bean cultivars carrying bc-1, bc-12, bc-2, and bc-22 alleles. The data suggest that bc-1 and bc-2 recessive resistance genes have no effect on the replication and cell-to-cell movement of BCMV, but affect systemic spread of BCMV in common bean. The BCMV resistance conferred by bc-1 and bc-2 and affecting systemic spread was found only partially effective when these two genes were expressed singly. The efficiency of the restriction of the systemic spread of the virus was greatly enhanced when the alleles of bc-1 and bc-2 genes were combined together.

scholarly journals The central and C-terminal domains of VPg of Clover yellow vein virus are important for VPg–HCPro and VPg–VPg interactions

2003 ◽  
Vol 84 (10) ◽  
pp. 2861-2869 ◽  
Author(s):  
Ma. Leonora M. Yambao ◽  
Chikara Masuta ◽  
Kenji Nakahara ◽  
Ichiro Uyeda
Keyword(s):  
Amino Acids ◽  
Western Blot ◽  
Yellow Vein ◽  
Transcription Activator ◽  
Yeast Two Hybrid ◽  
Yeast Two Hybrid System ◽  
Clover Yellow Vein Virus ◽  
Two Hybrid ◽  
Far Western Blot

Interactions between the major proteins of Clover yellow vein virus (ClYVV) were investigated using a GAL4 transcription activator-based yeast two-hybrid system (YTHS). Self-interactions manifested by VPg and HCPro and an interaction between NIb and NIaPro were observed in ClYVV. In addition, a strong HCPro–VPg interaction was detected by both YTHS and by in vitro far-Western blot analysis in ClYVV. A potyvirus HCPro–VPg interaction has not been reported previously. Using YTHS, domains in ClYVV for the VPg self-interaction and the HCPro–VPg interaction were mapped. The VPg C-terminal region (38 amino acids) was important for the VPg–VPg interaction and the central 19 amino acids were needed for the HCPro–VPg interaction.

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