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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Genetic inactivation of the transcription factor TIF- IA leads to nucleolar disruption, cell cycle arrest, and p53-mediated apoptosis.

Growth-dependent regulation of rRNA synthesis is mediated by TIF- IA, a basal transcription initiation factor for RNA polymerase I. We inactivated the murine TIF- IA gene by homologous recombination in mice and embryonic fibroblasts (MEFs). TIF- IA-/- embryos die before or at embryonic day 9.5 (E9.5), displaying retardation of growth and development. In MEFs, Cre-mediated depletion of TIF- IA leads to disruption of nucleoli, cell cycle arrest, upregulation of p53, and induction of apoptosis. Elevated levels of p53 after TIF- IA depletion are due to increased binding of ribosomal proteins, such as L11, to MDM2 and decreased interaction of MDM2 with p53 and p19(ARF). RNAi-induced loss of p53 overcomes proliferation arrest and apoptosis in response to TIF- IA ablation. The striking correlation between perturbation of nucleolar function, elevated levels of p53, and induction of cell suicide supports the view that the nucleolus is a stress sensor that regulates p53 activity.[1]

References

  1. Genetic inactivation of the transcription factor TIF-IA leads to nucleolar disruption, cell cycle arrest, and p53-mediated apoptosis. Yuan, X., Zhou, Y., Casanova, E., Chai, M., Kiss, E., Gröne, H.J., Schütz, G., Grummt, I. Mol. Cell (2005) [Pubmed]
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