Novel nucleolar pathway connecting intracellular energy status with p53 activation.
In response to a shortage of intracellular energy, mammalian cells reduce energy consumption and induce cell cycle arrest, both of which contribute to cell survival. Here we report that a novel nucleolar pathway involving the energy-dependent nucleolar silencing complex (eNoSC) and Myb-binding protein 1a (MYBBP1A) is implicated in these processes. Namely, in response to glucose starvation, eNoSC suppresses rRNA transcription, which results in a reduction in nucleolar RNA content. As a consequence, MYBBP1A, which is anchored to the nucleolus via RNA, translocates from the nucleolus to the nucleoplasm. The translocated MYBBP1A induces acetylation and accumulation of p53 by enhancing the interaction between p300 and p53, which eventually leads to the cell cycle arrest (or apoptosis). Taken together, our results indicate that the nucleolus works as a sensor that transduces the intracellular energy status into the cell cycle machinery.
Pubmed ID: 21471221 RIS Download
Acetylation | Apoptosis | Cell Line, Tumor | Cell Nucleolus | Energy Metabolism | Humans | Multiprotein Complexes | Nuclear Proteins | Nucleocytoplasmic Transport Proteins | Tumor Suppressor Protein p53 | p300-CBP Transcription Factors