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      Target of Rapamycin (TOR) in Nutrient Signaling and Growth Control

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      Author(s): * , 1 , † , 1
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      Publication date PMC-release:
      Journal: Genetics
      Publisher: Genetics Society of America

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          Abstract

          TOR ( Target Of Rapamycin) is a highly conserved protein kinase that is important in both fundamental and clinical biology. In fundamental biology, TOR is a nutrient-sensitive, central controller of cell growth and aging. In clinical biology, TOR is implicated in many diseases and is the target of the drug rapamycin used in three different therapeutic areas. The yeast Saccharomyces cerevisiae has played a prominent role in both the discovery of TOR and the elucidation of its function. Here we review the TOR signaling network in S. cerevisiae.

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          Transcriptional regulatory networks in Saccharomyces cerevisiae.

          T I Lee, Ziv Bar-Joseph (2002)
          We have determined how most of the transcriptional regulators encoded in the eukaryote Saccharomyces cerevisiae associate with genes across the genome in living cells. Just as maps of metabolic networks describe the potential pathways that may be used by a cell to accomplish metabolic processes, this network of regulator-gene interactions describes potential pathways yeast cells can use to regulate global gene expression programs. We use this information to identify network motifs, the simplest units of network architecture, and demonstrate that an automated process can use motifs to assemble a transcriptional regulatory network structure. Our results reveal that eukaryotic cellular functions are highly connected through networks of transcriptional regulators that regulate other transcriptional regulators.
          Article 0 comments Cited 769 times – based on 0 reviews     Review now
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            Dynamics and diversity in autophagy mechanisms: lessons from yeast.

            Hitoshi Nakatogawa, Kuninori Suzuki, Yoshiaki Kamada … (2009)
            Autophagy is a fundamental function of eukaryotic cells and is well conserved from yeast to humans. The most remarkable feature of autophagy is the synthesis of double membrane-bound compartments that sequester materials to be degraded in lytic compartments, a process that seems to be mechanistically distinct from conventional membrane traffic. The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today. Analyses of autophagy-related (Atg) proteins have unveiled dynamic and diverse aspects of mechanisms that underlie membrane formation during autophagy.
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              Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway.

              Pankaj Kapahi, Brian M. Zid, Tony Harper … (2004)
              In many species, reducing nutrient intake without causing malnutrition extends lifespan. Like DR (dietary restriction), modulation of genes in the insulin-signaling pathway, known to alter nutrient sensing, has been shown to extend lifespan in various species. In Drosophila, the target of rapamycin (TOR) and the insulin pathways have emerged as major regulators of growth and size. Hence we examined the role of TOR pathway genes in regulating lifespan by using Drosophila. We show that inhibition of TOR signaling pathway by alteration of the expression of genes in this nutrient-sensing pathway, which is conserved from yeast to human, extends lifespan in a manner that may overlap with known effects of dietary restriction on longevity. In Drosophila, TSC1 and TSC2 (tuberous sclerosis complex genes 1 and 2) act together to inhibit TOR (target of rapamycin), which mediates a signaling pathway that couples amino acid availability to S6 kinase, translation initiation, and growth. We find that overexpression of dTsc1, dTsc2, or dominant-negative forms of dTOR or dS6K all cause lifespan extension. Modulation of expression in the fat is sufficient for the lifespan-extension effects. The lifespan extensions are dependent on nutritional condition, suggesting a possible link between the TOR pathway and dietary restriction.
              Article 0 comments Cited 444 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                : Role: Communicating editor
                Journal
                Journal ID (nlm-ta): Genetics
                Journal ID (hwp): genetics
                Journal ID (pmc): genetics
                Journal ID (publisher-id): genetics
                Title: Genetics
                Publisher: Genetics Society of America
                ISSN (Print): 0016-6731
                ISSN (Electronic): 1943-2631
                Publication date (Print and electronic): December 2011
                Publication date (Print): December 2011
                Publication date PMC-release: December 2011
                Volume: 189
                Issue: 4
                Pages: 1177-1201
                Affiliations
                [* ]Department of Molecular Biology and National Centers of Competence in Research and Frontiers in Genetics and Chemical Biology, University of Geneva, Geneva, CH-1211, Switzerland
                [† ]Biozentrum, University of Basel, Basel CH-4056, Switzerland
                Author notes
                [1 ]Corresponding authors: Biozentrum, University of Basel, Klingelbergstrasse 70, Basel CH-4056, Switzerland. E-mail: m.hall@ 123456unibas.ch ; and Department of Molecular Biology, NCCRs Chemical Biology and Frontiers in Genetics, University of Geneva, 30 quai Ernest Ansermet Geneva CH-1211, Switzerland. E-mail: Robbie.Loewith@ 123456unige.ch
                Article
                Publisher ID: 133363
                DOI: 10.1534/genetics.111.133363
                PMC ID: 3241408
                PubMed ID: 22174183
                SO-VID: 4f9ea9fc-9e95-4247-8327-a6cb91e7cf60
                Copyright © Copyright © 2011 by the Genetics Society of America
                License:

                Available freely online through the author-supported open access option.

                History
                Date received : 29 July 2011
                Date accepted : 12 September 2011
                Categories
                Subject: YeastBook
                Subject: Cell Signaling & Development
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                ScienceOpen disciplines: Genetics
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                ScienceOpen disciplines: Genetics

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