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Overlapping functions of the pRb family in the regulation of rRNA synthesis

S Ciarmatori1, P H Scott, J E Sutcliffe

  • 1Division of Molecular Biology of the Cell II, German Cancer Research Centre, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.

Molecular and Cellular Biology
|August 4, 2001
PubMed

Insights

The pocket proteins pRb and p130 negatively regulate cell growth by controlling RNA polymerase I transcription. Disrupting the pRb family deregulates rRNA synthesis, indicating redundant control.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The pocket proteins pRb, p107, and p130 are known negative regulators of cell growth.
  • Previous research indicated that pRb overexpression can inhibit RNA polymerase I (Pol I) transcription.

Purpose of the Study:

  • To investigate whether pRb represses Pol I transcription under physiological conditions.
  • To determine the roles of pRb, p107, and p130 in regulating ribosomal RNA (rRNA) synthesis.

Main Methods:

  • Examined pre-rRNA levels in mouse cells lacking pRb alone or in combination with p107 and p130.
  • Assessed the impact of pRb family protein disruption on Pol I transcription.
  • Investigated the in vitro and in vivo effects of p130 overexpression on rRNA synthesis and UBF binding.

Main Results:

  • Pol I transcription was unaffected in pRb-knockout fibroblasts.
  • Disruption of the entire pRb family deregulated rRNA synthesis.
  • p130, but not p107, shares the ability with pRb to repress Pol I transcription.
  • rRNA production was abnormally elevated in Rb(-/-) p130(-/-) fibroblasts.
  • p130 overexpression inhibited an rRNA promoter and bound/inactivated the upstream binding factor (UBF).

Conclusions:

  • Endogenous pRb and p130 provide redundant control over rRNA synthesis.
  • p130 plays a significant role in repressing Pol I transcription, partly through UBF inactivation.
  • The pRb family, particularly p130, is crucial for regulating rRNA synthesis in living cells.

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