TORC1 signaling is governed by two negative regulators in fission yeast.
Identifieur interne : 000F76 ( Main/Corpus ); précédent : 000F75; suivant : 000F77TORC1 signaling is governed by two negative regulators in fission yeast.
Auteurs : Ning Ma ; Qingbin Liu ; Lili Zhang ; Elizabeth P. Henske ; Yan MaSource :
- Genetics [ 1943-2631 ] ; 2013.
English descriptors
- KwdEn :
- Amino Acid Sequence (MeSH), Amino Acid Transport Systems (metabolism), Amino Acids (genetics), Amino Acids (metabolism), Cell Cycle (MeSH), Gene Expression Regulation, Fungal (MeSH), Mechanistic Target of Rapamycin Complex 1 (MeSH), Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Mutation (MeSH), Receptors, Atrial Natriuretic Factor (genetics), Schizosaccharomyces (genetics), Schizosaccharomyces pombe Proteins (genetics), Schizosaccharomyces pombe Proteins (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , genetics : Amino Acids, Multiprotein Complexes, Receptors, Atrial Natriuretic Factor, Schizosaccharomyces pombe Proteins, TOR Serine-Threonine Kinases.
- chemical , metabolism : Amino Acid Transport Systems, Amino Acids, Multiprotein Complexes, Schizosaccharomyces pombe Proteins, TOR Serine-Threonine Kinases.
- genetics : Schizosaccharomyces.
- Amino Acid Sequence, Cell Cycle, Gene Expression Regulation, Fungal, Mechanistic Target of Rapamycin Complex 1, Mutation, Signal Transduction.
Abstract
The target of rapamycin (TOR) is a highly conserved protein kinase that regulates cell growth and metabolism. Here we performed a genome-wide screen to identify negative regulators of TOR complex 1 (TORC1) in Schizosaccharomyces pombe by isolating mutants that phenocopy Δtsc2, in which TORC1 signaling is known to be up-regulated. We discovered that Δnpr2 displayed similar phenotypes to Δtsc2 in terms of amino acid uptake defects and mislocalization of the Cat1 permease. However, Δnpr2 and Δtsc2 clearly showed different phenotypes in terms of rapamycin supersensitivity and Isp5 transcription upon various treatments. Furthermore, we showed that Tor2 controls amino acid homeostasis at the transcriptional and post-transcriptional levels. Our data reveal that both Npr2 and Tsc2 negatively regulate TORC1 signaling, and Npr2, but not Tsc2, may be involved in the feedback loop of a nutrient-sensing pathway.
DOI: 10.1534/genetics.113.154674
PubMed: 23934889
PubMed Central: PMC3781973
Links to Exploration step
pubmed:23934889Le document en format XML
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<term>Amino Acids (metabolism)</term>
<term>Cell Cycle (MeSH)</term>
<term>Gene Expression Regulation, Fungal (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Multiprotein Complexes (genetics)</term>
<term>Multiprotein Complexes (metabolism)</term>
<term>Mutation (MeSH)</term>
<term>Receptors, Atrial Natriuretic Factor (genetics)</term>
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<term>Schizosaccharomyces pombe Proteins (genetics)</term>
<term>Schizosaccharomyces pombe Proteins (metabolism)</term>
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<front><div type="abstract" xml:lang="en">The target of rapamycin (TOR) is a highly conserved protein kinase that regulates cell growth and metabolism. Here we performed a genome-wide screen to identify negative regulators of TOR complex 1 (TORC1) in Schizosaccharomyces pombe by isolating mutants that phenocopy Δtsc2, in which TORC1 signaling is known to be up-regulated. We discovered that Δnpr2 displayed similar phenotypes to Δtsc2 in terms of amino acid uptake defects and mislocalization of the Cat1 permease. However, Δnpr2 and Δtsc2 clearly showed different phenotypes in terms of rapamycin supersensitivity and Isp5 transcription upon various treatments. Furthermore, we showed that Tor2 controls amino acid homeostasis at the transcriptional and post-transcriptional levels. Our data reveal that both Npr2 and Tsc2 negatively regulate TORC1 signaling, and Npr2, but not Tsc2, may be involved in the feedback loop of a nutrient-sensing pathway. </div>
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<Abstract><AbstractText>The target of rapamycin (TOR) is a highly conserved protein kinase that regulates cell growth and metabolism. Here we performed a genome-wide screen to identify negative regulators of TOR complex 1 (TORC1) in Schizosaccharomyces pombe by isolating mutants that phenocopy Δtsc2, in which TORC1 signaling is known to be up-regulated. We discovered that Δnpr2 displayed similar phenotypes to Δtsc2 in terms of amino acid uptake defects and mislocalization of the Cat1 permease. However, Δnpr2 and Δtsc2 clearly showed different phenotypes in terms of rapamycin supersensitivity and Isp5 transcription upon various treatments. Furthermore, we showed that Tor2 controls amino acid homeostasis at the transcriptional and post-transcriptional levels. Our data reveal that both Npr2 and Tsc2 negatively regulate TORC1 signaling, and Npr2, but not Tsc2, may be involved in the feedback loop of a nutrient-sensing pathway. </AbstractText>
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<ReferenceList><Reference><Citation>Genes Dev. 2003 Aug 1;17(15):1829-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12869586</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging Cell. 2013 Aug;12(4):563-73</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23551936</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2004 Mar 26;279(13):12706-13</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14718525</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Methods Enzymol. 1983;101:202-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6310324</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 1991 Aug 23;253(5022):905-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">1715094</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Gene. 1993 Jan 15;123(1):127-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8422996</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 1993 May 7;73(3):585-96</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8387896</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 1995 Feb 23;373(6516):663-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7854443</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS Lett. 1995 Feb 13;359(2-3):215-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7867803</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1996 Dec;16(12):6752-64</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8943330</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Bacteriol. 1997 Oct;179(20):6325-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9335279</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genetics. 2005 Feb;169(2):539-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15466417</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2005 Apr 1;280(13):12231-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15657058</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2005 Apr 15;65(8):3336-46</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15833867</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Hum Mol Genet. 2005 Oct 1;14(19):2851-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16115814</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2007 Apr;27(8):3154-64</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17261596</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Cells. 2007 Dec;12(12):1357-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18076573</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2008 Jun 13;320(5882):1496-501</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18497260</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Genet Genomics. 2008 May;279(5):441-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18219492</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10314-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11504908</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genetics. 2002 Jul;161(3):1053-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12136010</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell. 2002 Jul;10(1):151-62</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12150915</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Cell Biol. 2002 Sep;4(9):648-57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12172553</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Biol Ther. 2003 May-Jun;2(3):222-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12878853</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Yeast. 2005 Oct 15;22(13):1013-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16200533</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14238-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16176982</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Microbiol. 2005 Nov;58(4):1074-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16262791</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genetics. 2006 Jun;173(2):569-78</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16624901</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Biol Cell. 2006 Nov;17(11):4790-800</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16928959</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Cells. 2006 Dec;11(12):1367-79</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17121544</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Metab. 2007 Jan;5(1):3-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17189200</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Cells. 2007 Feb;12(2):155-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17295836</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3514-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17360675</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem Soc Trans. 2009 Feb;37(Pt 1):217-22</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19143635</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2009 Mar 20;284(12):8023-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19150980</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Genet. 2009 Jun;5(6):e1000515</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19521502</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Cells. 2009 Aug;14(8):1015-28</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19624755</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Sci. 2009 Oct 15;122(Pt 20):3589-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19812304</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genetics. 2009 Oct;183(2):517-27</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19620394</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Microbiology. 2009 Dec;155(Pt 12):3816-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19778961</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Ann N Y Acad Sci. 2010 Jan;1184:87-105</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20146692</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Sci. 2010 Mar 1;123(Pt 5):777-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20144990</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS Lett. 2010 Apr 2;584(7):1327-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20036658</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2010 Apr 16;141(2):290-303</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20381137</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Biotechnol. 2010 Jun;28(6):617-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20473289</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2010 Oct 22;285(43):32818-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20729203</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Proteomics. 2011 Jun;10(6):M110.006478</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21454883</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Biol Cell. 2011 Nov;22(21):4124-33</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21900499</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2011 Nov 23;147(5):1104-17</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22118465</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2012 Apr 13;149(2):274-93</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22500797</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Sci. 2012 Apr 15;125(Pt 8):1920-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22344254</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2012 Jul 6;287(28):23434-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22661707</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Genet Genomics. 2012 Aug;287(8):651-62</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22806344</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2012 Nov;122(11):3807-16</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23114603</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Sci. 2012 Dec 1;125(Pt 23):5840-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22976295</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Biol. 2003 Aug 5;13(15):1259-68</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12906785</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
</record>
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