Nutritional Control of Cell Growth via TOR Signaling in Budding Yeast

Wei, Yuehua; Zheng, X.F. Steven

doi:10.1007/978-1-61779-173-4_18

Cited by 23 publications

(18 citation statements)

References 54 publications

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“…In yeast, activation of TOR in a nutrient-rich environment is responsible for directing a large part of cellular resources toward ribosome synthesis (38,63,65). The data obtained in this study suggest that inactivation of TOR not only stops the synthesis of new ribosomes, as previous studies have demonstrated (26,45,46), but also triggers extensive turnover of the existing ribosomes, resulting in a dramatic reduction of the cellular ribosome content.…”

Section: Discussionsupporting

confidence: 66%

“…n eukaryotic organisms from yeasts to humans, the conserved TOR signaling pathway plays the central role in regulating cellular responses to nutrient availability and mitogenic signals (4,65,67). Rapamycin is a potent TOR inhibitor that inhibits cell proliferation and growth (6, 68) and induces a number of coordinated changes in gene expression characteristic of starvation conditions (13, 24).…”

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confidence: 99%

“…The ribosome content dictates the cell's translational capacity and has long been known to correlate with the nutrient-controlled rate of exponential growth in microorganisms (29,36,51). Ribosome synthesis in Saccharomyces cerevisiae is activated in response to favorable growth conditions, largely through TOR-regulated increases in rRNA transcription and the expression of genes encoding ribosomal proteins and assembly factors, termed the RP and Ribi regulons (4,27,38,65). Conversely, inactivation of TOR causes repression of RP and Ribi gene expression and inhibits transcription and maturation of rRNAs (13,26,45,46,68), thereby causing an effective shutdown of ribosome biogenesis.…”

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confidence: 99%

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Rapid Cytoplasmic Turnover of Yeast Ribosomes in Response to Rapamycin Inhibition of TOR

Pestov

Shcherbik

2012

Molecular and Cellular Biology

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The target of rapamycin (TOR) pathway is the central regulator of cell growth in eukaryotes. Inhibition of TOR by rapamycin elicits changes in translation attributed mainly to altered translation initiation and repression of the synthesis of new ribosomes. Using quantitative analysis of rRNA, we found that the number of existing ribosomes present in a Saccharomyces cerevisiae culture during growth in rich medium rapidly decreases by 40 to 60% when the cells are treated with rapamycin. This process is not appreciably affected by a suppression of autophagy, previously implicated in degradation of ribosomes in eukaryotes upon starvation. Yeast cells deficient in the exosome function or lacking its cytoplasmic Ski cofactors show an abnormal pattern of rRNA degradation, particularly in the large ribosomal subunit, and accumulate rRNA fragments after rapamycin treatment and during diauxic shift. The exosome and Ski proteins are thus important for processing of rRNA decay intermediates, although they are probably not responsible for initiating rRNA decay. The role of cytoplasmic nucleases in rapamycin-induced rRNA degradation suggests mechanistic parallels of this process to nutrient-controlled ribosome turnover in prokaryotes. We propose that ribosome content is regulated dynamically in eukaryotes by TOR through both ribosome synthesis and the cytoplasmic turnover of mature ribosomes.

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Section: Discussionsupporting

confidence: 66%

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confidence: 99%

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confidence: 99%

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Rapid Cytoplasmic Turnover of Yeast Ribosomes in Response to Rapamycin Inhibition of TOR

Pestov

Shcherbik

2012

Molecular and Cellular Biology

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“…Exocytosis and autophagy are essential for a number of common biological processes, including; the immune response (Govind, 2008;Minty et al, 1983;Murray et al, 1998;Ostenson et al, 2006), cell growth (Brennwald & Rossi, 2007;Orlando & Guo, 2009;Wei & Zheng, 2011;Zhang et al, 2005), cell proliferation and apoptosis (Kundu, 2011;Shin et al, 2011;Zeng et al, 2012), and multicellular organism development (Gutnick et al, 2011;Hu et al, 2011;Sato & Sato, 2011;Tra et al, 2011). Autophagy and exocytosis both involve membrane trafficking and fusion events and so similar groups of molecular machinery may be required for both processes: such as GTPase proteins, that facilitate membrane tethering and SNARE proteins which are involved in membrane fusion.…”

Section: Exocytosis and Autophagy: Common Cellular Functions And Molementioning

confidence: 99%

At the Intersection of the Pathways for Exocytosis and Autophagy

Brooks¹,

Bader²,

Ng³

et al. 2012

Crosstalk and Integration of Membrane Trafficking Pathways

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“…7) They form two functionally distinct complexes termed TOR Complexes 1 (TORC1) and 2 (TORC2). 8,9) The signaling pathway through TORC1, which is sensitive to rapamycin treatment, promotes versatile processes leading to cell growth, including translation and ribosome biogenesis, 10) while it blocks autophagy and stress responses.…”

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confidence: 99%