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Virus variants with differences in the P1 protein coexist in a Plum pox virus population and display particular

Varvara I Maliogka1, Beatriz Salvador, Alberto Carbonell

  • 1Department of Plant Molecular Genetics, Centro Nacional de Biotecnología, Campus Universidad Autónoma de Madrid, 28049 Madrid, Spain.

Molecular Plant Pathology
|March 31, 2012
PubMed

Insights

Two amino acid changes in the P1 protein of Plum pox virus (PPV) significantly reduce its pathogenicity in woody hosts. These mutations, W29R and V139E, also influence symptom severity in herbaceous plants, highlighting P1 protein

Area of Science:

  • Plant virology
  • Molecular plant pathology
  • Potyviridae family

Background:

  • Plum pox virus (PPV) M-type isolates exhibit variable pathogenicity despite high sequence similarity.
  • A K109E substitution in the HCPro protein enhances PPV symptom severity and modifies infectivity in peach seedlings.
  • Mild PPV subisolates suggested the presence of unknown attenuating factors.

Purpose of the Study:

  • Investigate the role of P1 protein amino acid substitutions in PPV pathogenicity.
  • Determine the impact of specific P1 mutations on virus accumulation and symptom development in herbaceous and woody hosts.
  • Analyze the presence of these mutations in the original PPV-PS isolate.

Main Methods:

  • Site-directed mutagenesis to introduce W29R and V139E substitutions in the P1 protein.
  • Inoculation of herbaceous and woody hosts (Prunus persica) with mutated PPV.
  • Assessment of virus accumulation and symptom severity.
  • Deep sequencing of the original PPV-PS isolate.

Main Results:

  • W29R and V139E substitutions in P1 reduce virus accumulation and symptom severity in Prunus persica.
  • Concomitant W29R and V139E mutations abolish PPV infectivity in Prunus persica.
  • V139E substitution, but not W29R, attenuates symptoms in herbaceous hosts.
  • Deep sequencing revealed W29R and V139E heterogeneities in the original PPV-PS isolate.

Conclusions:

  • The P1 protein plays a crucial role in potyviral pathogenesis and host adaptation.
  • Specific amino acid substitutions in P1 modulate PPV pathogenicity in a host-dependent manner.
  • Viral populations exhibit complexity with pre-existing heterogeneities influencing pathogenicity.

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