Editors' ChoiceCell Cycle

Sensing Nucleolar Stress

Science's STKE  12 Jun 2001:
Vol. 2001, Issue 86, pp. tw6
DOI: 10.1126/stke.2001.86.tw6

The tumor suppressor protein p53 can induce cell-cycle arrest when cells are exposed to stressful conditions such as DNA damage or unregulated oncogene signaling. Nucleolar stress can now be added to that list. Pestov et al. report that functional p53 is required for a nucleolar protein called BOP (block of proliferation) to regulate rRNA synthesis and ribosome biogenesis. When a dominant negative form of BOP was expressed in fibroblasts, these nucleolar processes ceased, and cells did not proliferate. Simultaneous inhibition of p53 restored cell-cycle progression in these cells but did not affect the ribosomal events. The authors propose that a p53 pathway may monitor nucleolar function and link ribosome integrity to the cell cycle.

D. G. Pestov, S. Strezoska, L. F. Lau, Evidence of p53-dependent cross-talk between ribosome biogenesis and the cell cycle: Effects of nucleolar protein Bop1 on G1/S transition. Mol. Cell. Biol. 21, 4246-4255 (2001). [Abstract] [Full Text]