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BTG2 bridges PABPC1 RNA-binding domains and CAF1 deadenylase to control cell proliferation

Benjamin Stupfler1,2,3,4, Catherine Birck1,2,3,4, Bertrand Séraphin1,2,3,4

  • 1Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67404 Illkirch, France.

Nature Communications
|February 26, 2016
PubMed

Insights

The BTG2 protein directly interacts with poly(A)-binding protein PABPC1, revealing its mechanism for shortening mRNA poly(A) tails. This interaction is crucial for BTG2

Area of Science:

  • Molecular and Cellular Biology
  • Gene Regulation
  • Biochemistry

Background:

  • BTG2 (B-cell translocation gene 2) is implicated in cellular differentiation and cancer.
  • Its exact molecular function, particularly in mRNA regulation, remains elusive.
  • BTG2 interacts with the CAF1 deadenylase via its APRO domain.

Purpose of the Study:

  • To elucidate the molecular mechanism by which BTG2 influences mRNA poly(A) tail length.
  • To identify the specific protein interactions mediating BTG2's deadenylation activity.
  • To determine the role of BTG2-PABPC1 interaction in cell proliferation.

Main Methods:

  • In vitro biochemical assays to assess protein-protein interactions.
  • Analysis of the interaction between BTG2's APRO domain and PABPC1's RRM domain.
  • In vitro deadenylase activity assays using purified protein domains.

Main Results:

  • BTG2's APRO domain directly binds to the first RRM domain of PABPC1.
  • The isolated BTG2 APRO and PABPC1 RRM domains are sufficient to stimulate CAF1 deadenylase activity.
  • BTG2's interaction with PABPC1 RRM is essential for controlling cell proliferation.

Conclusions:

  • BTG2 directly stimulates mRNA deadenylation by interacting with PABPC1.
  • This interaction provides a direct mechanism for BTG2's role in poly(A) tail length control.
  • The BTG2-PABPC1 interaction is critical for regulating cell proliferation.

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