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Preferential replication of defective turnip yellow mosaic virus RNAs that express the 150-kDa protein in cis

T W Dreher1, J J Weiland

  • 1Department of Agricultural Chemistry, Oregon State University, Corvallis.

Archives of Virology. Supplementum
|January 1, 1994
PubMed

Insights

Turnip yellow mosaic virus RNA replication requires two essential proteins. While replication is typically cis-dependent, specific mutations allow for efficient trans-replication, suggesting a flexible viral replication complex.

Area of Science:

  • Virology
  • Molecular Biology
  • Plant Pathology

Background:

  • Turnip yellow mosaic virus (TYMV) replication is crucial for its life cycle.
  • Two viral proteins, 150-kDa and 70-kDa, are essential for RNA replication.
  • These proteins are proteolytically cleaved from a single precursor polypeptide.

Purpose of the Study:

  • To investigate the cis-preference of TYMV RNA replication.
  • To determine if mutations affecting essential replication proteins can be complemented in trans.
  • To elucidate the roles of the 150-kDa and 70-kDa proteins in viral RNA replication.

Main Methods:

  • Generating TYMV genomes with mutations in the 150-kDa and 70-kDa protein coding regions.
  • Assessing independent and trans-replication in turnip protoplasts.
  • Utilizing helper genomes and defective RNAs for complementation studies.

Main Results:

  • Mutations in essential replication protein genes rendered TYMV genomes defective for independent replication.
  • Most defective RNAs showed inefficient replication in trans.
  • A defective RNA with a large deletion in the 70-kDa protein gene was efficiently replicated in trans.
  • Defective RNAs with wild-type 150-kDa protein were replicated more efficiently in trans than those with wild-type 70-kDa protein.

Conclusions:

  • The cis-preference of TYMV RNA replication can be overcome under specific mutational conditions.
  • The 150-kDa and 70-kDa proteins likely form a stable complex on the viral RNA template.
  • This complex plays a critical role in the cis-acting replication mechanism of TYMV.

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