Biological characterization of French Potato virus Y (PVY) isolates collected from PVY-susceptible or -resistant tobacco plants possessing the recessive resistance gene va

2010 ◽  
Vol 59 (6) ◽  
pp. 1133-1143 ◽  
Author(s):  
C. Lacroix ◽  
L. Glais ◽  
C. Kerlan ◽  
J.-L. Verrier ◽  
E. Jacquot
2011 ◽  
Vol 60 (6) ◽  
pp. 1048-1054 ◽  
Author(s):  
C. Lacroix ◽  
L. Glais ◽  
J.-L. Verrier ◽  
C. Charlier ◽  
C. Lorencetti ◽  
...  

2002 ◽  
Vol 32 (6) ◽  
pp. 1067-1075 ◽  
Author(s):  
Sandrine Ruffel ◽  
Marie-Hélène Dussault ◽  
Alain Palloix ◽  
Benoît Moury ◽  
Abdelhafid Bendahmane ◽  
...  

1987 ◽  
Vol 38 (2) ◽  
pp. 395 ◽  
Author(s):  
R Heath ◽  
RJ Sward ◽  
JR Moran ◽  
AJ Mason ◽  
ND Hallam

Six potato virus Y isolates from Victoria and Queensland were characterized on the basis of host plant reactions. Four isolates from potato produced symptoms in indicator plants and potato cultivars consistent with those caused by the PVYO group. Two isolates from tobacco produced necrotic symptoms on some tobacco cultivars characteristic of the PVYN group, but did not systemically infect potato cultivars and therefore could not be considered to belong to any of the previously described PVY strain groups. Despite the wide variation in their biological characteristics, an antiserum produced to one of the potato isolates was able to detect all six of the isolates when used in ELISA


2014 ◽  
Vol 163 (7-8) ◽  
pp. 620-631 ◽  
Author(s):  
Jörg Schubert ◽  
Thomas Thieme ◽  
Ramona Thieme ◽  
Cuong Viet Ha ◽  
Giang Thi Hoang

VirusDisease ◽  
2021 ◽  
Author(s):  
Xuefeng Wei ◽  
Hongli Zheng ◽  
Yahan Chen ◽  
Si Zhang ◽  
Zhengnan Li ◽  
...  

2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 278-280
Author(s):  
J. Ptáček ◽  
P. Dědič ◽  
J. Matoušek

Fourteen Potato virus Y (PVY) isolates were characterized. They represented PVYN strain only. However, application of serological and molecular genetic methods led to a more complicated characterization. For example, five isolates induced necrotic symptoms on tobacco plants typical of PVY<sup>N</sup>, despite reacting as PVY<sup>O</sup> serologically. Moreover, the PVY isolates were not identical according to molecular genetic properties. Typical PVY<sup>NTN</sup> PCR products were observed for 11 isolates, but four of them (Hr220-5, Hr387-7, Nord 242 and Syn1Scot) did not produce potato tuber necrotic symptoms in infected cultivars. An immunocapture RT-PCR probing was developed using a set of 24 primer pairs derived from eight regions of the PVY genome. Using this method, five out of seven PVY<sup>NTN</sup> isolates including the Czech standard PVY<sup>NTN</sup> from the potato cv. Nicola were found to be identical. However, two PVY<sup>NTN</sup> isolates and all the other probed PVY samples showed unique patterns, suggesting specific differences at the nucleotide level. This method enabled specific identification of individual isolates variability even within different PVY strains.


2014 ◽  
Vol 159 (7) ◽  
pp. 1781-1785 ◽  
Author(s):  
Arturo Quintero-Ferrer ◽  
Loreto Robles-Hernandez ◽  
Ana C. Gonzalez-Franco ◽  
Camille Kerlan ◽  
Alexander V. Karasev

Plant Disease ◽  
2014 ◽  
Vol 98 (11) ◽  
pp. 1521-1529 ◽  
Author(s):  
B. Janzac ◽  
M. Tribodet ◽  
C. Lacroix ◽  
B. Moury ◽  
J. L. Verrier ◽  
...  

Emergence of viral genotypes can make control strategies based on resistance genes ineffective. A few years after the deployment of tobacco genotypes carrying alleles of the Potato virus Y (PVY) recessive resistance gene va, virulent PVY isolates have been reported, suggesting the low durability of va. To have a broader view of the evolutionary processes involved in PVY adaptation to va, we studied mutational pathways leading to the emergence of PVY resistance-breaking populations. The viral genome-linked protein (VPg) has been described to be potentially involved in va adaptation. Analyses of the VPg sequence of PVY isolates sampled from susceptible and resistant tobacco allowed us to identify mutations in the central part of the VPg. Analysis of the virulence of wild-type isolates with known VPg sequences and of mutated versions of PVY infectious clones allowed us to (i) validate VPg as the PVY virulence factor corresponding to va, (ii) highlight the fact that virulence gain in PVY occurs rapidly and preferentially by substitution at position AA105 in the VPg, and (iii) show that the 101G substitution in the VPg of a PVYC isolate is responsible for cross-virulence toward two resistance sources. Moreover, it appears that the evolutionary pathway of PVY adaptation to va depends on both virus and host genetic backgrounds.


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