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Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
08:26

Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins

Published on: August 31, 2017

Aberrant herpesvirus-induced polyadenylation correlates with cellular messenger RNA destruction

Yeon J Lee1, Britt A Glaunsinger

  • 1Department of Plant and Microbial Biology, University of California Berkeley, Berkeley, California, United States of America.

Plos Biology
|May 27, 2009
PubMed

Insights

Kaposi's sarcoma-associated herpesvirus (KSHV) SOX protein hijacks cellular polyadenylation, extending messenger RNA (mRNA) tails to trigger widespread mRNA destruction and block host gene expression.

Area of Science:

  • Molecular Biology
  • Virology
  • Gene Expression Regulation

Background:

  • Messenger RNA (mRNA) stability is crucial for controlling gene expression and cellular responses.
  • Herpesviruses often induce cellular mRNA destruction to suppress host gene expression and evade immunity.
  • The mechanism by which Kaposi's sarcoma-associated herpesvirus (KSHV) SOX protein induces mRNA turnover was previously unknown.

Purpose of the Study:

  • To elucidate the mechanism of KSHV SOX-induced mRNA turnover.
  • To investigate the role of polyadenylation in SOX-mediated host shutoff.
  • To identify cellular cofactors involved in SOX function.

Main Methods:

  • Analysis of poly(A) tail lengths in SOX-expressing cells.
  • Assessment of mRNA turnover rates upon inhibition of poly(A) tail formation.
  • Investigation of nuclear and cytoplasmic poly(A) binding protein localization and function.

Main Results:

  • KSHV SOX stimulates cellular transcriptome turnover through aberrant polyadenylation.
  • Transcripts in SOX-expressing cells exhibit extended poly(A) tails, linked to mRNA turnover.
  • Inhibition of poly(A) tail formation abrogates SOX's RNA turnover activity.
  • Nuclear relocalization of cytoplasmic poly(A) binding proteins is induced by SOX.

Conclusions:

  • KSHV SOX utilizes a novel mechanism of host shutoff by manipulating cellular polyadenylation.
  • SOX-induced aberrant polyadenylation drives accelerated mRNA turnover.
  • Cellular poly(A) binding proteins are essential cofactors for SOX-mediated host shutoff.
  • This study establishes a new model system for studying poly(A) tail-regulated mRNA turnover.

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