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Effects of Host-Adaptive Mutations on Hop Stunt Viroid Pathogenicity and Small RNA Biogenesis.

Zhixiang Zhang1, Changjian Xia1, Takahiro Matsuda2

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Five mutations in hop stunt viroid (HSVd) influence its infectivity and pathogenicity. These mutations alter hop stunt disease symptoms and impact small RNA profiles in infected plants.

Keywords:
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Area of Science:

  • Plant Pathology
  • Virology
  • Molecular Biology

Background:

  • Hop stunt viroid (HSVd) transmission from grapevine to hop has caused disease epidemics.
  • Convergent evolution resulted in HSVd-hop (HSVd-h) with five mutations compared to HSVd-grape (HSVd-g).
  • The biological significance of these five mutations remains uncharacterized.

Purpose of the Study:

  • To compare the biological properties of HSVd-g and HSVd-h.
  • To investigate the role of HSVd mutations in infectivity, replication, pathogenicity, and small RNA profiles.
  • To explore the potential involvement of host gene regulation in HSVd pathogenicity.

Main Methods:

  • Bioassays were conducted to assess infectivity, replication, and pathogenicity.
  • High-throughput sequencing was used to analyze HSVd-specific small RNAs (HSVd-sRNAs).
  • Site-directed mutagenesis was employed to evaluate specific mutation effects.

Main Results:

  • The five mutations are associated with differences in HSVd infectivity, replication, and pathogenicity.
  • HSVd-g induced more severe symptoms in cucumber than HSVd-h.
  • A mutation at position 54 in HSVd-g significantly increased pathogenicity.
  • HSVd-h infection led to specific down-regulation of adaptive nucleotide-containing sRNAs.
  • HSVd-sRNAs targeting cucumber genes were identified, but direct correlation with symptom severity was not observed.
  • Expression of cucumber genes ERF011 and GTL2 was altered by HSVd infection.

Conclusions:

  • The five mutations acquired during HSVd evolution play a crucial role in modulating viroid-host interactions.
  • HSVd pathogenicity is influenced by specific mutations and altered host gene expression, particularly ERF011 and GTL2.
  • Further research is needed to elucidate the precise mechanisms linking these host genes to HSVd-induced disease.