Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2001 Jun;14(6):707-14.
doi: 10.1094/MPMI.2001.14.6.707.

Mutations in pea seedborne mosaic virus genome-linked protein VPg after pathotype-specific virulence in Pisum sativum

B Borgstrøm  1 , I E Johansen
Affiliations
Free article

Mutations in pea seedborne mosaic virus genome-linked protein VPg after pathotype-specific virulence in Pisum sativum

B Borgstrøm et al. Mol Plant Microbe Interact. 2001 Jun.
Free article

Abstract

Pisum sativum plant introduction (PI) line 269818 is resistant to potyvirus pea seedborne mosaic virus (PSbMV) isolates, categorized as pathotype P1, and is susceptible to pathotype P4 isolates. This difference in infectivity is determined by the viral genome-linked protein (VPg) cistron. Mutational analysis of VPg of PSbMV isolates DPD1 and NY representing pathotypes P1 and P4 revealed that codon changes affecting amino acids 105 to 117 in the central region of VPg influenced virulence on PI 269818. In contrast, infectivity on pea cultivar Dark Skinned Perfection, which is susceptible to both pathotypes, was not affected by the mutations. Mutants overcoming resistance in PI 269818 were analyzed for changes in the VPg coding region upon passage through PI 269818 and Dark Skinned Perfection. Adaptive changes were observed only upon passage through PI 269818 and only at codons from amino acid 105 to 117. Expression of DPD1 VPg in PI 269818 did not affect infection by NY, which suggests that VPg from DPD1 is not an elicitor of a general resistance response. The results are compatible with the hypothesis that viral amplification depends upon the interaction between VPg and a host factor.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

LinkOut - more resources