AI Article Synopsis

  • The study explores how plant resistance affects viral fitness and leads to the emergence of resistance-breaking strains, particularly in potyviruses like the papaya ringspot virus (PRSV).
  • The research identifies specific mutations in the VPg protein of PRSV that allow it to evade interaction with the primary resistance factor, eIF4E, while instead engaging with a different version called eIF(iso)4E.
  • The findings highlight potential targets for breeding watermelon plants that can resist these newly adapted viral strains, enhancing crop protection.

Article Abstract

Plant resistance, which acts as a selective pressure that affects viral population fitness, leads to the emergence of resistance-breaking virus strains. Most recessive resistance to potyviruses is related to the mutation of eukaryotic translation initiation factor 4E (eIF4E) or its isoforms that break their interactions with the viral genome-linked protein (VPg). In this study, we found that the VPg α1-α2 loop, which is essential for binding eIF4E, is the most variable domain of papaya ringspot virus (PRSV) VPg. PRSV VPg with the naturally occurring amino acid substitution of K105Q or E108G in the α1-α2 loop fails to interact with watermelon (Citrullus lanatus) eIF4E but interacts with watermelon eIF(iso)4E instead. Moreover, PRSV carrying these mutations can break the eIF4E-mediated resistance to PRSV in watermelon accession PI 244019. We further revealed that watermelon eIF(iso)4E with the amino acid substitutions of DNQS to GAAA in the cap-binding pocket could not interact with PRSV VPg with natural amino acid substitution of K105Q or E108G. Therefore, our finding provides a precise target for engineering watermelon germplasm resistant to resistance-breaking PRSV isolates.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11588673PMC
http://dx.doi.org/10.1111/mpp.70033DOI Listing

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