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Polysome Fractionation and Analysis of Mammalian Translatomes on a Genome-wide Scale
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A mechanism for translationally coupled mRNA turnover: interaction between the poly(A) tail and a c-fos RNA coding

C Grosset1, C Y Chen, N Xu

  • 1Department of Biochemistry and Molecular Biology, The University of Texas Houston Medical School 77030, USA.

Cell
|October 29, 2000
PubMed

Insights

The major protein-coding-region determinant of instability (mCRD) in c-fos mRNA relies on its distance from the poly(A) tail. A protein complex involving Unr, PABP, PAIP-1, hnRNP D, and NSAP1 stabilizes mRNA by blocking deadenylation.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • RNA Metabolism

Background:

  • mRNA turnover is crucial for gene expression regulation.
  • The major protein-coding-region determinant of instability (mCRD) in the c-fos proto-oncogene transcript influences mRNA stability.
  • Understanding the mechanisms of mRNA decay is essential for comprehending cellular processes.

Purpose of the Study:

  • To investigate the role of the mCRD in mRNA turnover.
  • To identify proteins associated with the mCRD and their function.
  • To elucidate the interplay between mRNA turnover and translation.

Main Methods:

  • Identification of mCRD-associated proteins using biochemical techniques.
  • Analysis of mRNA stability in response to protein complex modulation.
  • Investigating the impact of mCRD distance from the poly(A) tail on its function.

Main Results:

  • The function of mCRD is dependent on its proximity to the poly(A) tail.
  • Five proteins (Unr, PABP, PAIP-1, hnRNP D, NSAP1) were identified as mCRD-associated proteins, forming a multiprotein complex.
  • Overexpression of these proteins stabilized mCRD-containing mRNA by inhibiting deadenylation.

Conclusions:

  • A bridging complex forms between the poly(A) tail and the mCRD.
  • Ribosome transit disrupts or reorganizes this complex, leading to mRNA deadenylation and decay.
  • This study reveals a novel mechanism of mRNA regulation involving translation-dependent decay mediated by the mCRD.

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