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Alternative poly(A) site utilization during adenovirus infection coincides with a decrease in the activity of a

K P Mann1, E A Weiss, J R Nevins

  • 1Section of Genetics, Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina.

Molecular and Cellular Biology
|April 1, 1993
PubMed
Summary
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Polyadenylation site selection in adenovirus infection is regulated by the processing factor CF1. Reduced CF1 activity and unstable binding to the L1 poly(A) site during late infection phases explain its decreased utilization.

Area of Science:

  • Molecular Biology
  • Virology
  • Gene Regulation

Background:

  • Polyadenylation is a crucial step in mRNA biogenesis, involving the addition of a poly(A) tail to pre-mRNA.
  • Poly(A) site usage can be a regulatory mechanism, as observed during adenovirus infections.
  • Adenovirus major late transcription unit exhibits differential poly(A) site usage between early and late infection phases.

Purpose of the Study:

  • To investigate the role of the CF1 processing factor in regulating poly(A) site selection during adenovirus infection.
  • To determine the molecular basis for the differential usage of L1 and L3 poly(A) sites in adenovirus.

Main Methods:

  • Comparative analysis of CF1 binding stability to L1 and L3 poly(A) sites.
  • Assay of CF1 activity levels during different stages of adenovirus infection.

Related Experiment Videos

Main Results:

  • The interaction of CF1 with the L1 poly(A) site is less stable compared to the L3 poly(A) site.
  • A significant decrease in CF1 activity is observed as adenovirus infection progresses to the late phase.
  • These findings correlate with the reduced utilization of the L1 poly(A) site during late-stage infection.

Conclusions:

  • Reduced CF1 activity and less stable CF1-L1 poly(A) site interaction contribute to the decreased use of the L1 poly(A) site in late-stage adenovirus infection.
  • Poly(A) site selection is a key regulatory point influenced by processing factor dynamics during viral replication.