Mycoreovirus genome rearrangements associated with RNA silencing deficiency

Ana Eusebio-Cope1, Nobuhiro Suzuki2

  • 1Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama 710-0046, Japan.

Nucleic Acids Research
|March 25, 2015
PubMed

Insights

RNA silencing in fungi suppresses genome rearrangements in Mycoreovirus 1 (MyRV1). Deficiencies in host RNA silencing components increased MyRV1 genome alterations, particularly in specific viral and host strain combinations.

Area of Science:

  • Mycology
  • Virology
  • Molecular Biology

Background:

  • Mycoreovirus 1 (MyRV1) is a double-stranded RNA virus infecting the chestnut blight fungus Cryphonectria parasitica.
  • MyRV1 confers hypovirulence, a reduced virulence phenotype.
  • Viral protein p29, encoded by Cryphonectria hypovirus 1, is known to induce MyRV1 genome rearrangements and suppress RNA silencing.

Purpose of the Study:

  • To investigate the role of the host RNA silencing pathway in suppressing MyRV1 genome rearrangements.
  • To determine if defects in host RNA silencing components affect the frequency of MyRV1 genome rearrangements.

Main Methods:

  • Utilized wild-type and mutant strains of MyRV1 and Cryphonectria parasitica.
  • Employed host strains with deletions in RNA silencing genes (dicer-like [dcl] and argonaute-like [agl]).
  • Infected host strains with a MyRV1 S4 internal deletion mutant (MyRV1/S4ss).

Main Results:

  • Intragenic rearrangements, including duplication of segments S1, S2, and S3, occurred more frequently in RNA silencing-deficient host strains (Δdcl2 and Δagl2) infected with MyRV1/S4ss.
  • Increased rearrangement frequency was specific to the MyRV1/S4ss and Δdcl2/Δagl2 strain combinations.
  • Genome rearrangement generation required longer culture periods in Δagl2 compared to Δdcl2.

Conclusions:

  • Host RNA silencing plays a suppressive role in preventing genome rearrangements of double-stranded RNA viruses like MyRV1.
  • Specific interactions between viral and host genetic components influence the rate of viral genome instability.

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