Journal articles: 'Torz'

1

Gon, Stéphanie, Jean-Claude Patte, Vincent Méjean, and Chantal Iobbi-Nivol. "The torYZ (yecK bisZ) Operon Encodes a Third Respiratory Trimethylamine N-Oxide Reductase inEscherichia coli." Journal of Bacteriology 182, no. 20 (October 15, 2000): 5779–86. http://dx.doi.org/10.1128/jb.182.20.5779-5786.2000.

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ABSTRACT The bisZ gene of Escherichia coli was previously described as encoding a minor biotin sulfoxide (BSO) reductase in addition to the main cytoplasmic BSO reductase, BisC. In this study, bisZ has been renamed torZ based on the findings that (i) the torZ gene product, TorZ, is able to reduce trimethylamine N-oxide (TMAO) more efficiently than BSO; (ii) although TorZ is more homologous to BisC than to the TMAO reductase TorA (63 and 42% identity, respectively), it is located mainly in the periplasm as is TorA; (iii)torZ belongs to the torYZ operon, and the first gene, torY (formerly yecK), encodes a pentahemic c-type cytochrome homologous to the TorC cytochrome of the TorCAD respiratory system. Furthermore, the torYZ operon encodes a third TMAO respiratory system, with catalytic properties that are clearly different from those of the TorCAD and the DmsABC systems. ThetorYZ and the torCAD operons may have diverged from a common ancestor, but, surprisingly, notorD homologue is found in the sequences aroundtorYZ. Moreover, the torYZ operon is expressed at very low levels under the conditions tested, and, in contrast to torCAD, it is not induced by TMAO or dimethyl sulfoxide.

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Bordi, Christophe, Chantal Iobbi-Nivol, Vincent Méjean, and Jean-Claude Patte. "Effects of ISSo2 Insertions in Structural and Regulatory Genes of the Trimethylamine Oxide Reductase of Shewanella oneidensis." Journal of Bacteriology 185, no. 6 (March 15, 2003): 2042–45. http://dx.doi.org/10.1128/jb.185.6.2042-2045.2003.

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ABSTRACT We have isolated three Shewanella oneidensis mutants specifically impaired in trimethylamine oxide (TMAO) respiration. The mutations arose from insertions of an ISSo2 element into torA, torR, and torS, encoding, respectively, the TMAO reductase TorA, the response regulator TorR, and the sensor TorS. Although TorA is not the sole enzyme reducing TMAO in S. oneidensis, growth analysis showed that it is the main respiratory TMAO reductase. Use of a plasmid-borne torE′-lacZ fusion confirmed that the TorS-TorR phosphorelay mediates TMAO induction of the torECAD operon.

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3

Gregorová, Jana, Lýdia Chovancová, Zuzana Ondrejková, and Alexandra Škrinárová. "Obnova torz architektúry ako špecializovaná architektonická disciplína." Archaeologia historica, no. 1 (2015): 7–39. http://dx.doi.org/10.5817/ah2015-1-1.

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4

Sturgill, Thomas W., Adiel Cohen, Melanie Diefenbacher, Mark Trautwein, Dietmar E. Martin, and Michael N. Hall. "TOR1 and TOR2 Have Distinct Locations in Live Cells." Eukaryotic Cell 7, no. 10 (August 22, 2008): 1819–30. http://dx.doi.org/10.1128/ec.00088-08.

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ABSTRACT TOR is a structurally and functionally conserved Ser/Thr kinase found in two multiprotein complexes that regulate many cellular processes to control cell growth. Although extensively studied, the localization of TOR is still ambiguous, possibly because endogenous TOR in live cells has not been examined. Here, we examined the localization of green fluorescent protein (GFP) tagged, endogenous TOR1 and TOR2 in live S. cerevisiae cells. A DNA cassette encoding three copies of green fluorescent protein (3XGFP) was inserted in the TOR1 gene (at codon D330) or the TOR2 gene (at codon N321). The TORs were tagged internally because TOR1 or TOR2 tagged at the N or C terminus was not functional. The TOR1 D330-3XGFP strain was not hypersensitive to rapamycin, was not cold sensitive, and was not resistant to manganese toxicity caused by the loss of Pmr1, all indications that TOR1-3XGFP was expressed and functional. TOR2-3XGFP was functional, as TOR2 is an essential gene and TOR2 N321-3XGFP haploid cells were viable. Thus, TOR1 and TOR2 retain function after the insertion of 748 amino acids in a variable region of their noncatalytic domain. The localization patterns of TOR1-3XGFP and TOR2-3XGFP were documented by imaging of live cells. TOR1-3XGFP was diffusely cytoplasmic and concentrated near the vacuolar membrane. The TOR2-3XGFP signal was cytoplasmic but predominately in dots at the plasma membrane. Thus, TOR1 and TOR2 have distinct localization patterns, consistent with the regulation of cellular processes as part of two different complexes.

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5

Bordi, Christophe, Mireille Ansaldi, Stéphanie Gon, Cécile Jourlin-Castelli, Chantal Iobbi-Nivol, and Vincent Méjean. "Genes Regulated by TorR, the Trimethylamine Oxide Response Regulator of Shewanella oneidensis." Journal of Bacteriology 186, no. 14 (July 15, 2004): 4502–9. http://dx.doi.org/10.1128/jb.186.14.4502-4509.2004.

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ABSTRACT The torECAD operon encoding the trimethylamine oxide (TMAO) respiratory system of Shewanella oneidensis is positively controlled by the TorS/TorR two-component system when TMAO is available. Activation of the tor operon occurs upon binding of the phosphorylated response regulator TorR to a single operator site containing the direct repeat nucleotide sequence TTCATAN4TTCATA. Here we show that the replacement of any nucleotide of one TTCATA hexamer prevented TorR binding in vitro, meaning that TorR specifically interacts with this DNA target. Identical direct repeat sequences were found in the promoter regions of torR and of the new gene torF (SO4694), and they allowed TorR binding to both promoters. Real-time PCR experiments revealed that torR is negatively autoregulated, whereas torF is strongly induced by TorR in response to TMAO. Transcription start site location and footprinting analysis indicate that the operator site at torR overlaps the promoter −10 box, whereas the operator site at torF is centered at −74 bp from the start site, in agreement with the opposite role of TorR in the regulation of the two genes. Since torF and torECAD are positively coregulated by TorR, we propose that the TorF protein plays a role related to TMAO respiration.

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6

Saldivia, Manuel, Antonio Barquilla, Jean-Mathieu Bart, Rosario Diaz-González, Michael N. Hall, and Miguel Navarro. "Target of rapamycin (TOR) kinase in Trypanosoma brucei: an extended family." Biochemical Society Transactions 41, no. 4 (July 18, 2013): 934–38. http://dx.doi.org/10.1042/bst20130052.

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The complex life cycle of Trypanosoma brucei provides an excellent model system to understand signalling pathways that regulate development. We described previously the classical functions of TOR (target of rapamycin) 1 and TOR2 in T. brucei. In a more recent study, we described a novel TOR kinase, named TOR4, which regulates differentiation from the proliferative infective form to the quiescent form. In contrast with TOR1 loss-of-function, down-regulation of TOR4 triggers an irreversible differentiation process through the development of the insect pre-adapted quiescent form. TOR4 governs a signalling pathway distinct from those controlled by the conventional TOR complexes TORC1 and TORC2. Depletion of TOR4 induces all well-known characteristics of the quiescent developmental stage in trypanosomes, including expression of the PAD (proteins associated with differentiation) surface proteins and transcriptional down-regulation of the VSG (variant surface glycoprotein) gene. TOR4 kinase forms a structurally and functionally distinct complex named TORC4. TOR4 associates with LST8 (lethal with sec-13 protein 8) and other factors including an armadillo-domain-containing protein and the major vault protein, which probably serves as a scaffold for this kinase. Research in T. brucei, a protozoan parasite that diverged from the eukaryotic tree early in evolution, may help to uncover new functions of TOR kinases.

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7

Ansaldi, Mireille, Gwénola Simon, Michèle Lepelletier, and Vincent Méjean. "The TorR High-Affinity Binding Site Plays a Key Role in Both torR Autoregulation and torCADOperon Expression in Escherichia coli." Journal of Bacteriology 182, no. 4 (February 15, 2000): 961–66. http://dx.doi.org/10.1128/jb.182.4.961-966.2000.

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ABSTRACT In the presence of trimethylamine N-oxide (TMAO), the TorS-TorR two-component regulatory system induces thetorCAD operon, which encodes the TMAO respiratory system ofEscherichia coli. The sensor protein TorS detects TMAO and transphosphorylates the response regulator TorR which, in turn, activates transcription of torCAD. The torRgene and the torCAD operon are divergently transcribed, and the short torR-torC intergenic region contains four direct repeats (the tor boxes) which proved to be TorR binding sites. The tor box 1-box 2 region covers thetorR transcription start site and constitutes a TorR high-affinity binding site, whereas box 3 and box 4 correspond to low-affinity binding sites. By using torR-lacZ operon fusions in different genetic backgrounds, we showed that thetorR gene is negatively autoregulated. Surprisingly, TorR autoregulation is TMAO independent and still occurs in atorS mutant. In addition, this negative regulation involves only the TorR high-affinity binding site. Together, these data suggest that phosphorylated as well as unphosphorylated TorR binds the box 1-box 2 region in vivo, thus preventing RNA polymerase from binding to the torR promoter whatever the growth conditions. By changing the spacing between box 2 and box 3, we demonstrated that the DNA motifs of the high- and low-affinity binding sites must be close to each other and located on the same side of the DNA helix to allow induction of the torCAD operon. Thus, prior TorR binding to the box 1-box 2 region seems to allow cooperative binding of phosphorylated TorR to box 3 and box 4.

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8

Matsuo, Tomohiko, Yoko Otsubo, Jun Urano, Fuyuhiko Tamanoi, and Masayuki Yamamoto. "Loss of the TOR Kinase Tor2 Mimics Nitrogen Starvation and Activates the Sexual Development Pathway in Fission Yeast." Molecular and Cellular Biology 27, no. 8 (January 29, 2007): 3154–64. http://dx.doi.org/10.1128/mcb.01039-06.

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ABSTRACT Fission yeast has two TOR (target of rapamycin) kinases, namely Tor1 and Tor2. Tor1 is required for survival under stressed conditions, proper G1 arrest, and sexual development. In contrast, Tor2 is essential for growth. To analyze the functions of Tor2, we constructed two temperature-sensitive tor2 mutants. Interestingly, at the restrictive temperature, these mutants mimicked nitrogen starvation by arresting the cell cycle in G1 phase and initiating sexual development. Microarray analysis indicated that expression of nitrogen starvation-responsive genes was induced extensively when Tor2 function was suppressed, suggesting that Tor2 normally mediates a signal from the nitrogen source. As with mammalian and budding yeast TOR, we find that fission yeast TOR also forms multiprotein complexes analogous to TORC1 and TORC2. The raptor homologue, Mip1, likely forms a complex predominantly with Tor2, producing TORC1. The rictor/Avo3 homologue, Ste20, and the Avo1 homologue, Sin1, appear to form TORC2 mainly with Tor1 but may also bind Tor2. The Lst8 homologue, Wat1, binds to both Tor1 and Tor2. Our analysis shows, with respect to promotion of G1 arrest and sexual development, that the loss of Tor1 (TORC2) and the loss of Tor2 (TORC1) exhibit opposite effects. This highlights an intriguing functional relationship among TOR kinase complexes in the fission yeast Schizosaccharomyces pombe.

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9

Csiba, László. "Thoughts on „defensive” medicine." Orvosi Hetilap 148, no. 12 (March 1, 2007): 531–34. http://dx.doi.org/10.1556/oh.2007.27965.

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„Önvédelmi” orvostan kifejezés alatt azt a torz diagnosztikus és terápiás orvosi magatartást értjük, amikor az orvos az egzisztenciáját, munkáját érintő fenyegetettség miatt egyes beavatkozásokat nem mer elvégezni, másrészt „túlbiztosítja” magát és felesleges vizsgálatokat végeztet belső bizonytalansága, a beteg bizalmatlansága vagy az ellenséges társadalmi környezet miatt. A beteg és orvos közti bizalmat legsúlyosabban a lelkiismeretlen orvosok visszaélései károsítják, ezeket a média felnagyítja. Az orvos-beteg kapcsolat nem degradálható szerződéses jogviszonnyá. A fiatal orvosokat meg kell ismertetni a sikeres diagnózis személyiséget gazdagító örömével. Legyen egészséges önbizalmuk, merjék vállalni a diagnosztikus és terápiás kihívásokat. Valamennyiünknek küzdeni kell az orvosellenes társadalmi hangulat és azon okok ellen, melyek az „önvédelmi” orvostan gyakorlatát előidézték és erősítették.

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10

Kamada, Yoshiaki, Yuko Fujioka, Nobuo N. Suzuki, Fuyuhiko Inagaki, Stephan Wullschleger, Robbie Loewith, Michael N. Hall, and Yoshinori Ohsumi. "Tor2 Directly Phosphorylates the AGC Kinase Ypk2 To Regulate Actin Polarization." Molecular and Cellular Biology 25, no. 16 (August 15, 2005): 7239–48. http://dx.doi.org/10.1128/mcb.25.16.7239-7248.2005.

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ABSTRACT The target of rapamycin (TOR) protein kinases, Tor1 and Tor2, form two distinct complexes (TOR complex 1 and 2) in the yeast Saccharomyces cerevisiae. TOR complex 2 (TORC2) contains Tor2 but not Tor1 and controls polarity of the actin cytoskeleton via the Rho1/Pkc1/MAPK cell integrity cascade. Substrates of TORC2 and how TORC2 regulates the cell integrity pathway are not well understood. Screening for multicopy suppressors of tor2, we obtained a plasmid expressing an N-terminally truncated Ypk2 protein kinase. This truncation appears to partially disrupt an autoinhibitory domain in Ypk2, and a point mutation in this region (Ypk2D239A) conferred upon full-length Ypk2 the ability to rescue growth of cells compromised in TORC2, but not TORC1, function. YPK2 D239A also suppressed the lethality of tor2Δ cells, suggesting that Ypks play an essential role in TORC2 signaling. Ypk2 is phosphorylated directly by Tor2 in vitro, and Ypk2 activity is largely reduced in tor2Δ cells. In contrast, Ypk2D239A has increased and TOR2-independent activity in vivo. Thus, we propose that Ypk protein kinases are direct and essential targets of TORC2, coupling TORC2 to the cell integrity cascade.

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11

Roggiani, Manuela, and Mark Goulian. "Oxygen-Dependent Cell-to-Cell Variability in the Output of the Escherichia coli Tor Phosphorelay." Journal of Bacteriology 197, no. 12 (March 30, 2015): 1976–87. http://dx.doi.org/10.1128/jb.00074-15.

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ABSTRACTEscherichia colisenses and responds to trimethylamine-N-oxide (TMAO) in the environment through the TorT-TorS-TorR signal transduction system. The periplasmic protein TorT binds TMAO and stimulates the hybrid kinase TorS to phosphorylate the response regulator TorR through a phosphorelay. Phosphorylated TorR, in turn, activates transcription of thetorCADoperon, which encodes the proteins required for anaerobic respiration via reduction of TMAO to trimethylamine. Interestingly,E. colirespires TMAO in both the presence and absence of oxygen, a behavior that is markedly different from the utilization of other alternative electron acceptors by this bacterium. Here we describe an unusual form of regulation by oxygen for this system. While the average level oftorCADtranscription is the same for aerobic and anaerobic cultures containing TMAO, the behavior across the population of cells is strikingly different under the two growth conditions. Cellular levels oftorCADtranscription in aerobic cultures are highly heterogeneous, in contrast to the relatively homogeneous distribution in anaerobic cultures. Thus, oxygen regulates the variance of the output but not the mean for the Tor system. We further show that this oxygen-dependent variability stems from the phosphorelay.IMPORTANCETrimethylamine-N-oxide (TMAO) is utilized by numerous bacteria as an electron acceptor for anaerobic respiration. InE. coli, expression of the proteins required for TMAO respiration is tightly regulated by a signal transduction system that is activated by TMAO. Curiously, although oxygen is the energetically preferred electron acceptor, TMAO is respired even in the presence of oxygen. Here we describe an interesting and unexpected form of regulation for this system in which oxygen produces highly variable expression of the TMAO utilization proteins across a population of cells without affecting the mean expression of these proteins. To our knowledge, this is the first reported example of a stimulus regulating the variance but not the mean output of a signaling system.

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12

Barbet, N. C., U. Schneider, S. B. Helliwell, I. Stansfield, M. F. Tuite, and M. N. Hall. "TOR controls translation initiation and early G1 progression in yeast." Molecular Biology of the Cell 7, no. 1 (January 1996): 25–42. http://dx.doi.org/10.1091/mbc.7.1.25.

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Saccharomyces cerevisiae cells treated with the immunosuppressant rapamycin or depleted for the targets of rapamycin TOR1 and TOR2 arrest growth in the early G1 phase of the cell cycle. Loss of TOR function also causes an early inhibition of translation initiation and induces several other physiological changes characteristic of starved cells entering stationary phase (G0). A G1 cyclin mRNA whose translational control is altered by substitution of the UBI4 5' leader region (UBI4 is normally translated under starvation conditions) suppresses the rapamycin-induced G1 arrest and confers starvation sensitivity. These results suggest that the block in translation initiation is a direct consequence of loss of TOR function and the cause of the G1 arrest. We propose that the TORs, two related phosphatidylinositol kinase homologues, are part of a novel signaling pathway that activates eIF-4E-dependent protein synthesis and, thereby, G1 progression in response to nutrient availability. Such a pathway may constitute a checkpoint that prevents early G1 progression and growth in the absence of nutrients.

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13

Gon, Stéphanie, Marie-Thérèse Giudici-Orticoni, Vincent Méjean, and Chantal Iobbi-Nivol. "Electron Transfer and Binding of thec-Type Cytochrome TorC to the TrimethylamineN-Oxide Reductase inEscherichia coli." Journal of Biological Chemistry 276, no. 15 (October 30, 2000): 11545–51. http://dx.doi.org/10.1074/jbc.m008875200.

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Reduction of trimethylamineN-oxide (E′0(TMAO/TMA)= +130 mV) inEscherichia coliis carried out by the Tor system, an electron transfer chain encoded by thetorCADoperon and made up of the periplasmic terminal reductase TorA and the membrane-anchored pentahemicc-type cytochrome TorC. Although the role of TorA in the reduction of trimethylamineN-oxide (TMAO) has been clearly established, no direct evidence for TorC involvement has been presented. TorC belongs to the NirT/NapCc-type cytochrome family based on homologies of its N-terminal tetrahemic domain (TorCN) to the cytochromes of this family, but TorC contains a C-terminal extension (TorCC) with an additional heme-binding site. In this study, we show that both domains are required for the anaerobic bacterial growth with TMAO. The intact TorC protein and its two domains, TorCNand TorCC, were produced independently and purified for a biochemical characterization. The reduced form of TorC exhibited visible absorption maxima at 552, 523, and 417 nm. Mediated redox potentiometry of the heme centers of the purified components identified two negative midpoint potentials (−177 and −98 mV) localized in the tetrahemic TorCNand one positive midpoint potential (+120 mV) in the monohemic TorCC. In agreement with these values, thein vitroreconstitution of electron transfer between TorC, TorCN, or TorCCand TorA showed that only TorC and TorCCwere capable of electron transfer to TorA. Surprisingly, interaction studies revealed that only TorC and TorCNstrongly bind TorA. Therefore, TorCCdirectly transfers electrons to TorA, whereas TorCN, which probably receives electrons from the menaquinone pool, is involved in both the electron transfer to TorCCand the binding to TorA.

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Alarcon, Clara M., Joseph Heitman, and Maria E. Cardenas. "Protein Kinase Activity and Identification of a Toxic Effector Domain of the Target of Rapamycin TOR Proteins in Yeast." Molecular Biology of the Cell 10, no. 8 (August 1999): 2531–46. http://dx.doi.org/10.1091/mbc.10.8.2531.

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In complex with FKBP12, the immunosuppressant rapamycin binds to and inhibits the yeast TOR1 and TOR2 proteins and the mammalian homologue mTOR/FRAP/RAFT1. The TOR proteins promote cell cycle progression in yeast and human cells by regulating translation and polarization of the actin cytoskeleton. A C-terminal domain of the TOR proteins shares identity with protein and lipid kinases, but only one substrate (PHAS-I), and no regulators of the TOR-signaling cascade have been identified. We report here that yeast TOR1 has an intrinsic protein kinase activity capable of phosphorylating PHAS-1, and this activity is abolished by an active site mutation and inhibited by FKBP12-rapamycin or wortmannin. We find that an intact TOR1 kinase domain is essential for TOR1 functions in yeast. Overexpression of a TOR1 kinase-inactive mutant, or of a central region of the TOR proteins distinct from the FRB and kinase domains, was toxic in yeast, and overexpression of wild-type TOR1 suppressed this toxic effect. Expression of the TOR-toxic domain leads to a G1 cell cycle arrest, consistent with an inhibition of TOR function in translation. Overexpression of the PLC1gene, which encodes the yeast phospholipase C homologue, suppressed growth inhibition by the TOR-toxic domains. In conclusion, our findings identify a toxic effector domain of the TOR proteins that may interact with substrates or regulators of the TOR kinase cascade and that shares sequence identity with other PIK family members, including ATR, Rad3, Mei-41, and ATM.

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15

Semchyshyn, Halyna. "Reactive Carbonyls Induce TOR- and Carbohydrate-Dependent Hormetic Response in Yeast." Scientific World Journal 2020 (March 12, 2020): 1–6. http://dx.doi.org/10.1155/2020/4275194.

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The induction of the beneficial and detrimental effects by reactive carbonyl species in yeast has been investigated. In this study, we have presented evidence that glyoxal and methylglyoxal at low concentrations were able to induce a hormetic adaptive response in glucose-grown but not fructose-grown yeast. The hormetic effect was also TOR-dependent. The mutation in genes encoding either TOR1 or TOR2 protein makes yeast highly sensitive to both α-dicarbonyls studied. Simultaneous disruption of TOR1 and TOR2 resulted in higher yeast sensitivity to the α-dicarbonyls as compared to parental cells, but double mutant survived better under carbonyl stress than its single mutant counterparts. The data obtained are consistent with the previous works which reported high toxicity of the α-dicarbonyls and extend them with the report on the beneficial TOR-dependent hormetic effect of glyoxal and methylglyoxal.

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Glant, Tibor. "amerikai felsőoktatásról, magyar szemmel." Gerundium 11, no. 1-2 (June 30, 2020): 238–51. http://dx.doi.org/10.29116/gerundium/2020/1-2/19.

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Ma Magyarországon vajmi keveset tudunk az amerikai felsőoktatásról, annak történetéről és problémáiról. Ez nagymértékben a kommunista örökségnek tudható be, hiszen 1945/47 és 1989 között az amerikanisztika a „tűrt” es a „tiltott” közti szürke zónába szorult. Ezért az amerikai felsőoktatásról alkotott képünk túlzottan is támaszkodik a média torz tükrére (filmek, apokaliptikus tudósítások). Tanulmányunkban először ránézünk a számokra és a rendszer működésére (állami és magánegyetemek, tandíj, a sport szerepe stb.), áttekintjük a felsőfokú oktatás történetét és preferenciait a gyarmati kortól napjainkig, majd röviden felvázoljuk, hogy látták, mit is mondtak ugyanerről azok a magyar utazók, akik ezt 1945 előtt még szabadon megtehették. Ezt követően elemezzük a jelenleg folyó vitákat és azok politikai dimenzióit. Zárásként – személyes tapasztalatok alapján –értékeljük a jelenlegi helyzetet, és felvázoljuk a felsőoktatással kapcsolatos problémák szerepét a jelenlegi elnökválasztási kampányban.

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Yanagida, Mitsuhiro, Nobuyasu Ikai, Mizuki Shimanuki, and Kenichi Sajiki. "Nutrient limitations alter cell division control and chromosome segregation through growth-related kinases and phosphatases." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1584 (December 27, 2011): 3508–20. http://dx.doi.org/10.1098/rstb.2011.0124.

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In dividing fission yeast Schizosaccharomyces pombe cells, the balance between Wee1 kinase and Cdc25 phosphatase which control the cyclin-dependent kinase (CDK) at the G2–M transition determines the rod-shaped cell length. Under nitrogen source starvation or glucose limitation, however, cell size determination is considerably modulated, and cell size shortening occurs for wild-type cells. For several mutants of kinases or phosphatases, including CDK, target of rapamycin complex (TORC) 1 and 2, stress-responsive mitogen-activated protein kinase (MAPK) Sty1/Spc1, MAPK kinase Wis1, calcium- and calmodulin-dependent protein kinase kinase-like Ssp1, and type 2A and 2A-related phosphatases inhibitor Sds23, this cell shortening does not normally occur. In tor1 and ssp1 mutants, cell elongation is observed. Sds23 that binds to and inhibits 2A and 2A-related phosphatases is synergistic with Ssp1 in the cell size determination and survival under low glucose and nitrogen source. Tor2 (TORC1) is required for growth, whereas Tor1 (TORC2) is needed for determining division size according to different nutrient conditions. Surprisingly, in growth-diminished tor2 mutant or rapamycin-treated cells, the requirement of separase/Cut1-securin/Cut2 essential for chromosome segregation is greatly alleviated. By contrast, defects of tor1 with secruin/ cut2 or overproduction of Cut1 are additive. While Tor1 and Tor2 are opposite in their apparent functions, both may actually coordinate cell division with growth in response to the changes in nutrients.

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Helliwell, Stephen B., Isabelle Howald, Nik Barbet, and Michael N. Hall. "TOR2 Is Part of Two Related Signaling Pathways Coordinating Cell Growth in Saccharomyces cerevisiae." Genetics 148, no. 1 (January 1, 1998): 99–112. http://dx.doi.org/10.1093/genetics/148.1.99.

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Abstract The Saccharomyces cerevisiae genes TOR1 and TOR2 encode phosphatidylinositol kinase homologs. TOR2 has two essential functions. One function overlaps with TOR1 and mediates protein synthesis and cell cycle progression. The second essential function of TOR2 is unique to TOR2 and mediates the cell-cycle-dependent organization of the actin cytoskeleton. We have isolated temperature-sensitive mutants that are defective for either one or both of the two TOR2 functions. The three classes of mutants were as follows. Class A mutants, lacking only the TOR2-unique function, are defective in actin cytoskeleton organization and arrest within two to three generations as small-budded cells in the G2/M phase of the cell cycle. Class B mutants, lacking only the TOR-shared function, and class C mutants, lacking both functions, exhibit a rapid loss of protein synthesis and a G1 arrest within one generation. To define further the two functions of TOR2, we isolated multicopy suppressors that rescue the class A or B mutants. Overexpression of MSS4, PKC1, PLC1, RHO2, ROM2, or SUR1 suppressed the growth defect of a class A mutant. Surprisingly, overexpression of PLC1 and MSS4 also suppressed the growth defect of a class B mutant. These genes encode proteins that are involved in phosphoinositide metabolism and signaling. Thus, the two functions (readouts) of TOR2 appear to involve two related signaling pathways controlling cell growth.

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Helliwell, S. B., P. Wagner, J. Kunz, M. Deuter-Reinhard, R. Henriquez, and M. N. Hall. "TOR1 and TOR2 are structurally and functionally similar but not identical phosphatidylinositol kinase homologues in yeast." Molecular Biology of the Cell 5, no. 1 (January 1994): 105–18. http://dx.doi.org/10.1091/mbc.5.1.105.

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The Saccharomyces cerevisiae genes TOR1 and TOR2 were originally identified by mutations that confer resistance to the immunosuppressant rapamycin. TOR2 was previously shown to encode an essential 282-kDa phosphatidylinositol kinase (PI kinase) homologue. The TOR1 gene product is also a large (281 kDa) PI kinase homologue, with 67% identity to TOR2. TOR1 is not essential, but a TOR1 TOR2 double disruption uniquely confers a cell cycle (G1) arrest as does exposure to rapamycin; disruption of TOR2 alone is lethal but does not cause a cell cycle arrest. TOR1-TOR2 and TOR2-TOR1 hybrids indicate that carboxy-terminal domains of TOR1 and TOR2 containing a lipid kinase sequence motif are interchangeable and therefore functionally equivalent; the other portions of TOR1 and TOR2 are not interchangeable. The TOR1-1 and TOR2-1 mutations, which confer rapamycin resistance, alter the same potential protein kinase C site in the respective protein's lipid kinase domain. Thus, TOR1 and TOR2 are likely similar but not identical, rapamycin-sensitive PI kinases possibly regulated by phosphorylation. TOR1 and TOR2 may be components of a novel signal transduction pathway controlling progression through G1.

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Genest, Olivier, Marianne Ilbert, Vincent Méjean, and Chantal Iobbi-Nivol. "TorD, an Essential Chaperone for TorA Molybdoenzyme Maturation at High Temperature." Journal of Biological Chemistry 280, no. 16 (February 21, 2005): 15644–48. http://dx.doi.org/10.1074/jbc.m501119200.

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TorD has been recognized as an accessory protein that improves maturation of TorA, the molybdenum cofactor-containing trimethylamine oxide reductase ofEscherichia coli. In this study, we show that at 42 °C and in the absence of TorD TorA is poorly matured and almost completely degraded. Strikingly, TorD restores TorA maturation to the same level whatever the growth temperature.In vitroexperiments in which apoTorA was incubated with or without TorD at various temperatures confirm that TorD is an essential chaperone for TorA at elevated temperatures preventing apoTorA mis-folding before cofactor insertion.

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Felkai, Péter, and László Gorove. "The basic considerations on patient repatriation." Orvosi Hetilap 150, no. 35 (August 1, 2009): 1671–78. http://dx.doi.org/10.1556/oh.2009.28627.

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A beteg jólléte mindenekelőtt! – ezt az elvet sem a társadalmi, sem a politikai nyomás, sem az adminisztrációs kötelezettségek, sem a kereskedelmi érdekek nem sérthetik az orvosi rendtartás előírása szerint. A mindennapi, repatriációval összefüggő orvosi és nem orvosi tevékenységek azonban ezt az elvet gyakran megszegik. A hazai gyakorlatban az utazási biztosítások alapján történő beteg-hazaszállításoknak komoly anomáliái vannak. Ha ezeknek az eredete a financiális szempontok felülkerekedése a beteg érdekének rovására, akkor ezt a motivációs tényezőt azonnal ki kell iktatni! A torz gyakorlatot (többek között) a hosszú távú, betegszállítással kapcsolatos szakmai szabályok hiánya teszi lehetővé. Elsősorban a repatriáció szakmai indikációinak hiánya, a szállíthatósággal kapcsolatos hiányos állásfoglalások, következésképpen a szakmai felelősség elmosása nyújt erre lehetőséget. A szakmai szabályok hiánya lehetetlenné teszi a hazaszállítással megbízott egészségügyi szolgáltató számára a szakmai szempontok betartását – és ezzel a beteg érdekeinek érvényesítését. A helyzetet rontja, hogy a klinikai szakmák képviselői és maguk az alapellátásban dolgozó orvosok is alig ismerik a beteg hazaszállításának szakmai kérdéseit, annak gyakorlati lebonyolítását. Jelen közleményben a szerzők összefoglalják a repatriáció indikációit és kontraindikációit, útmutatást adnak a szállíthatóság kérdésének eldöntéséhez. Részletesen ismertetik a hazaszállításra alkalmazható járműveket, azok használatának korlátait.

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Gon, Stéphanie, Jean-Claude Patte, Jean-Philippe Dos Santos, and Vincent Méjean. "Reconstitution of the Trimethylamine Oxide Reductase Regulatory Elements of Shewanella oneidensis in Escherichia coli." Journal of Bacteriology 184, no. 5 (March 1, 2002): 1262–69. http://dx.doi.org/10.1128/jb.184.5.1262-1269.2002.

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ABSTRACT Several bacteria can grow by using small organic compounds such as trimethylamine oxide (TMAO) as electron acceptors. In Shewanella species, the TMAO reductase respiratory system is encoded by the torECAD operon. We showed that production of the TMAO reductase of S. oneidensis was induced by TMAO and repressed by oxygen, and we noticed that a three-gene cluster (torSTR) encoding a complex two-component regulatory system was present downstream of the torECAD operon. We introduced the torSTR gene cluster into Escherichia coli and showed that this regulatory gene cluster is involved in TMAO induction of the torE promoter but plays no role in the oxygen control. The TorR response regulator was purified, and gel shift and footprinting experiments revealed that TorR binds to a single region located about 70 bases upstream of the transcription start site of the tor structural operon. By deletion analysis, we confirmed that the TorR operator site is required for induction of the tor structural promoter. As the TMAO regulatory system of S. oneidensis is homologous to that of E. coli, we investigated a possible complementation between the TMAO regulatory components of the two bacteria. Interestingly, TorSec, the TMAO sensor of E. coli, was able to transphosphorylate TorRso, the TMAO response regulator of S. oneidensis.

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Ilbert, Marianne, Vincent Méjean, and Chantal Iobbi-Nivol. "Functional and structural analysis of members of the TorD family, a large chaperone family dedicated to molybdoproteins." Microbiology 150, no. 4 (April 1, 2004): 935–43. http://dx.doi.org/10.1099/mic.0.26909-0.

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The trimethylamine N-oxide (TMAO) reductase TorA, a DMSO reductase family member, is a periplasmic molybdoenzyme of Escherichia coli. The cytoplasmic protein TorD acts as a chaperone for TorA, allowing the efficient insertion of the molybdenum cofactor into the apoform of the enzyme prior to its secretion. This paper demonstrates that TorD is a member of a large family of prokaryotic proteins that are structurally related. Moreover, their genes generally belong to operons also encoding molybdoenzymes of the DMSO reductase family. Both the TorD and the DMSO reductase families present a similar phylogenetic organization, suggesting a co-evolution of these two families of proteins. This hypothesis is also supported by the fact that the TorD and DmsD chaperones cannot replace each other and thus appear dedicated to specific molybdopartners. Interestingly, it was found that the positive effect of TorD on TorA maturation, and the partial inhibitory effect of DmsD and homologues, are independent of the TorA signal sequence.

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Ansaldi, Mireille, Cécile Jourlin-Castelli, Michèle Lepelletier, Laurence Théraulaz, and Vincent Méjean. "Rapid Dephosphorylation of the TorR Response Regulator by the TorS Unorthodox Sensor in Escherichia coli." Journal of Bacteriology 183, no. 8 (April 15, 2001): 2691–95. http://dx.doi.org/10.1128/jb.183.8.2691-2695.2001.

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ABSTRACT Induction of the torCAD operon, encoding the trimethylamine N-oxide (TMAO) respiratory system, is tightly controlled by the TorS-TorR phosphorelay system in response to TMAO availability. TorS is an unorthodox sensor that contains three phosphorylation sites and transphosphorylates TorR via a four-step phosphorelay, His443→Asp723→His850→Asp(TorR). In this study, we provide genetic evidence that TorS can dephosphorylate phospho-TorR when TMAO is removed. Dephosphorylation probably occurs by a reverse phosphorelay, Asp(TorR)→His850→Asp723, since His850 and Asp723 are both essential in this process. By using reverse transcriptase PCR, we also show that TMAO removal results in shutoff of toroperon transcription in less than 2 min. Based on our results and on analogy to other phosphorelay signal transduction systems, we propose that reverse phosphotransfer could be a rapid and efficient mechanism to inactivate response regulators.

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Dow, Jennifer M., Frank Gabel, Frank Sargent, and Tracy Palmer. "Characterization of a pre-export enzyme–chaperone complex on the twin-arginine transport pathway." Biochemical Journal 452, no. 1 (April 25, 2013): 57–66. http://dx.doi.org/10.1042/bj20121832.

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The Tat (twin-arginine translocation) system is a protein targeting pathway utilized by prokaryotes and chloroplasts. Tat substrates are produced with distinctive N-terminal signal peptides and are translocated as fully folded proteins. In Escherichia coli, Tat-dependent proteins often contain redox cofactors that must be loaded before translocation. Trimethylamine N-oxide reductase (TorA) is a model bacterial Tat substrate and is a molybdenum cofactor-dependent enzyme. Co-ordination of cofactor loading and translocation of TorA is directed by the TorD protein, which is a cytoplasmic chaperone known to interact physically with the TorA signal peptide. In the present study, a pre-export TorAD complex has been characterized using biochemical and biophysical techniques, including SAXS (small-angle X-ray scattering). A stable, cofactor-free TorAD complex was isolated, which revealed a 1:1 binding stoichiometry. Surprisingly, a TorAD complex with similar architecture can be isolated in the complete absence of the 39-residue TorA signal peptide. The present study demonstrates that two high-affinity binding sites for TorD are present on TorA, and that a single TorD protein binds both of those simultaneously. Further characterization suggested that the C-terminal ‘Domain IV’ of TorA remained solvent-exposed in the cofactor-free pre-export TorAD complex. It is possible that correct folding of Domain IV upon cofactor loading is the trigger for TorD release and subsequent export of TorA.

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Bossak-Herbst, Barbara. "Etnograficzny portret publiczności warszawskich wyścigów konnych." Przegląd Socjologii Jakościowej 14, no. 2 (August 28, 2018): 6–28. http://dx.doi.org/10.18778/1733-8069.14.2.01.

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Tekst zawiera portret stałej publiczności wyścigów konnych na Torze Służewiec w Warszawie. W oparciu o materiały zebrane podczas długotrwałej obserwacji etnograficznej scharakteryzowana została subkultura stałych uczestników mitingów wyścigowych, ich zachowania przestrzenne, niewerbalne i językowe. Kategorie uwrażliwiające zaczerpnięte z dorobku Ervinga Goffmana pozwoliły wyeksponować uwzorowania ich zachowań. Publiczność wyścigowa nigdy dotąd nie była przedmiotem dociekań badaczy społecznych w Polsce. Artykuł ukazuje różne płaszczyzny, na których można zarysować typologię współczesnych stałych i regularnych bywalców Toru Służewiec. Punktem odniesienia dla niej były badania etnograficzne bywalców wyścigowych Kate Fox w Wielkiej Brytanii oraz Johna Rosecrance w Stanach Zjednoczonych. Osią tekstu jest teza, iż Tor Służewiec jest wyjątkową niszą społeczną zdominowaną przez przeważnie starszych mężczyzn, którzy poprzez zrytualizowane i wymagające zaangażowanie uczestniczą w hazardzie, znajdują swoją podmiotowość i poczucie przynależności.

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Epple, Sandra, Fabienne Roche, and Stefan Brandenburg. "The Sooner the Better: Drivers’ Reactions to Two-Step Take-Over Requests in Highly Automated Driving." Proceedings of the Human Factors and Ergonomics Society Annual Meeting 62, no. 1 (September 2018): 1883–87. http://dx.doi.org/10.1177/1541931218621428.

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Driving behavior after take-over requests (TORs) is one of the most popular subjects in human factors re-search on highly automated driving. Many studies utilized one-step TOR procedures to prompt drivers to resume vehicle control. The present paper examines driver behavior when experiencing a two-step TOR procedure in different modalities. A two-step TOR gives drivers a choice to resume vehicle controls be-tween a warning (first step) and an alarm (second step). Our findings indicate that a substantial number of drivers resumes vehicle controls after the second step, resulting in a higher number of crashes. More generally, criticality of the driving situation increases with increasing reaction times. Driving and interview data suggest that step two of the TOR should be presented earlier. Alternatively, a multi-step TOR could be used to increase drivers’ situational awareness. Auditory TORs are associated with shorter reaction times than visual-auditory TORs. Implications on TOR design are discussed.

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Hölper, Julia E., Barbara G. Klupp, G. W. Gant Luxton, Kati Franzke, and Thomas C. Mettenleiter. "Function of Torsin AAA+ ATPases in Pseudorabies Virus Nuclear Egress." Cells 9, no. 3 (March 17, 2020): 738. http://dx.doi.org/10.3390/cells9030738.

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Newly assembled herpesvirus nucleocapsids traverse the intact nuclear envelope by a vesicle-mediated nucleo-cytoplasmic transport for final virion maturation in the cytoplasm. For this, they bud at the inner nuclear membrane resulting in primary enveloped particles in the perinuclear space (PNS) followed by fusion of the primary envelope with the outer nuclear membrane (ONM). While the conserved viral nuclear egress complex orchestrates the first steps, effectors of fusion of the primary virion envelope with the ONM are still mostly enigmatic but might include cellular proteins like SUN2 or ESCRT-III components. Here, we analyzed the influence of the only known AAA+ ATPases located in the endoplasmic reticulum and the PNS, the Torsins (Tor), on nuclear egress of the alphaherpesvirus pseudorabies virus. For this overexpression of wild type and mutant proteins as well as CRISPR/Cas9 genome editing was applied. Neither single overexpression nor gene knockout (KO) of TorA or TorB had a significant impact. However, TorA/B double KO cells showed decreased viral titers at early time points of infection and an accumulation of primary virions in the PNS pointing to a delay in capsid release during nuclear egress.

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Michniewicz, Aleksandra. "Tors in Central European Mountains – are they indicators of past environments?" Bulletin of Geography. Physical Geography Series 16, no. 1 (June 18, 2019): 67–87. http://dx.doi.org/10.2478/bgeo-2019-0005.

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Abstract Tors represent one of the most characteristic landforms in the uplands and mountains of Central Europe, including the Sudetes, Czech-Moravian Highlands, Šumava/Bayerischer Wald, Fichtelgebirge or Harz. These features occur in a range of lithologies, although granites and gneisses are particularly prone to tor formation. Various models of tor formation and development have been presented, and for each model the tors were thought to have evolved under specific environmental conditions. The two most common theories emphasised their progressive emergence from pre-Quaternary weathering mantles in a two-stage scenario, and their development across slopes under periglacial conditions in a one-stage scenario. More recently, tors have been analysed in relation to ice sheet extent, the selectivity of glacial erosion, and the preservation of landforms under ice. In this paper we describe tor distribution across Central Europe along with hypotheses relating to their formation and development, arguing that specific evolutionary histories are not supported by unequivocal evidence and that the scenarios presented were invariably model-driven. Several examples from the Sudetes are presented to demonstrate that tor morphology is strongly controlled by lithology and structure. The juxtaposition of tors of different types is not necessarily evidence that they differ in their mode of origin or age. Pathways of tor remodelling and degradation under subaerial conditions are identified and it is argued that processes of tor formation and development are ongoing. Thus, tors are not reliable indicators of past environments, because they are considerably influenced by both geological factors, such as lithology and structure, and geomorphological factors such as hillslope setting..

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Hálová, Lenka, Wei Du, Sara Kirkham, Duncan L. Smith, and Janni Petersen. "Phosphorylation of the TOR ATP binding domain by AGC kinase constitutes a novel mode of TOR inhibition." Journal of Cell Biology 203, no. 4 (November 18, 2013): 595–604. http://dx.doi.org/10.1083/jcb.201305103.

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TOR (target of rapamycin) signaling coordinates cell growth, metabolism, and cell division through tight control of signaling via two complexes, TORC1 and TORC2. Here, we show that fission yeast TOR kinases and mTOR are phosphorylated on an evolutionarily conserved residue of their ATP-binding domain. The Gad8 kinase (AKT homologue) phosphorylates fission yeast Tor1 at this threonine (T1972) to reduce activity. A T1972A mutation that blocked phosphorylation increased Tor1 activity and stress resistance. Nitrogen starvation of fission yeast inhibited TOR signaling to arrest cell cycle progression in G1 phase and promoted sexual differentiation. Starvation and a Gad8/T1972-dependent decrease in Tor1 (TORC2) activity was essential for efficient cell cycle arrest and differentiation. Experiments in human cell lines recapitulated these yeast observations, as mTOR was phosphorylated on T2173 in an AKT-dependent manner. In addition, a T2173A mutation increased mTOR activity. Thus, TOR kinase activity can be reduced through AGC kinase–controlled phosphorylation to generate physiologically significant changes in TOR signaling.

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Schonbrun, Miriam, Dana Laor, Luis López-Maury, Jürg Bähler, Martin Kupiec, and Ronit Weisman. "TOR Complex 2 Controls Gene Silencing, Telomere Length Maintenance, and Survival under DNA-Damaging Conditions." Molecular and Cellular Biology 29, no. 16 (June 22, 2009): 4584–94. http://dx.doi.org/10.1128/mcb.01879-08.

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ABSTRACT The Target Of Rapamycin (TOR) kinase belongs to the highly conserved eukaryotic family of phosphatidylinositol-3-kinase-related kinases (PIKKs). TOR proteins are found at the core of two distinct evolutionarily conserved complexes, TORC1 and TORC2. Disruption of TORC1 or TORC2 results in characteristically dissimilar phenotypes. TORC1 is a major cell growth regulator, while the cellular roles of TORC2 are not well understood. In the fission yeast Schizosaccharomyces pombe, Tor1 is a component of the TORC2 complex, which is particularly required during starvation and various stress conditions. Our genome-wide gene expression analysis of Δtor1 mutants indicates an extensive similarity with chromatin structure mutants. Consistently, TORC2 regulates several chromatin-mediated functions, including gene silencing, telomere length maintenance, and tolerance to DNA damage. These novel cellular roles of TORC2 are rapamycin insensitive. Cells lacking Tor1 are highly sensitive to the DNA-damaging drugs hydroxyurea (HU) and methyl methanesulfonate, similar to mutants of the checkpoint kinase Rad3 (ATR). Unlike Rad3, Tor1 is not required for the cell cycle arrest in the presence of damaged DNA. Instead, Tor1 becomes essential for dephosphorylation and reactivation of the cyclin-dependent kinase Cdc2, thus allowing reentry into mitosis following recovery from DNA replication arrest. Taken together, our data highlight critical roles for TORC2 in chromatin metabolism and in promoting mitotic entry, most notably after recovery from DNA-damaging conditions. These data place TOR proteins in line with other PIKK members, such as ATM and ATR, as guardians of genome stability.

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Zboiński, Krzysztof, and Milena Gołofit-Stawińska. "Wstęp do analizy dynamiki pojazdu szynowego w krzywych przejściowych przy prędkościach większych od krytycznej." Rail Vehicles, no. 3 (July 2, 2013): 5–12. http://dx.doi.org/10.53502/rail-139363.

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Artykuł przedstawia dyskusję autorów dotyczącą celowości podjęcia usystematyzowanego badania dynamiki ruchu pojazdów szynowych w krzywych przejściowych przy prędkościach większych od krytycznej. Pomimo tego, że pojazdy szynowe budowane są tak aby ich prędkość eksploatacyjna była mniejsza od prędkości krytycznej (dla prędkości większych zachowanie modelu pojazdu reprezentowane jest przez rozwiązania stateczne okresowe), badania stateczności ruchu tak w torze prostym jak i łuku kołowym są nieustannie prowadzone. Przyczyną są nie tak rzadkie przypadki kiedy pojazd może poruszać się z prędkością większą od krytycznej. Interesującym dla autorów zagadnieniem są własności dynamiczne układu na odcinkach toru umiejscowionych pomiędzy jest prostą i łukiem kołowym, tzn. w krzywych przejściowych. Trzeba tylko uzmysłowić sobie kluczową różnicę formalną w tym przypadku. Jest nią tutaj ciągła zmiana promienia krzywizny i przechyłki toru. W konsekwencji, nie można tu oczekiwać rozwiązań statecznych stacjonarnych i statecznych okresowych, tak typowych dla analiz stateczności w torze prostym i łukach kołowych.

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Shida, Yoshisada, and Viktoriya Kan. "How Effective Are Special Economic Zones in the Russian Far East: A Financial Assessment Using Firm-Level Data." Spatial Economics 17, no. 1 (2021): 35–65. http://dx.doi.org/10.14530/se.2021.1.035-065.

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With ‘Advanced Development Zones (TORs)’ formed in the Russian Far East in the mid-2010s, now it is a good time to overview the first five years of this policy development. Here, in contrast to the mostly qualitative prior studies, we assess the initial growth of the Far East TORs quantitatively. In order to achieve this, we set up a novel financial database which we use to trace the dynamics of zonal economic activities, compare their fiscal performances, and capture their structural differences. Our analysis, based on the database composing resident registers and financial accounting reports, reveals the following. First, a few TORs successfully attract new residents, leading to regional heterogeneity of the resident distribution and zone development dynamics. Second, there is one or a few companies in each TOR that dominate in the zone and determine total TOR revenue. Thus, their presences sway the TORs’ economic performance. Curiously, these ‘dominant’ firms do not necessarily act as ‘anchor residents’ originally supposed to initiate foundations of clusters in their industries. Third, small businesses, on the contrast, show rather low profitability; however, there is variation among companies in different TORs. SMEs are hoped to play a key role in creating local labor market stability and adding to the regional economy what centralized big business cannot. In this regard, the TOR’s institutional improvement is vital to ensure local SME profitability. Summing up, we bid to label TORs as having ‘rich’ or ‘poor’ development potential to attract and stimulate SME in the zones

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Cruz, M. Cristina, Lora M. Cavallo, Jenifer M. Görlach, Gary Cox, John R. Perfect, Maria E. Cardenas, and Joseph Heitman. "Rapamycin Antifungal Action Is Mediated via Conserved Complexes with FKBP12 and TOR Kinase Homologs inCryptococcus neoformans." Molecular and Cellular Biology 19, no. 6 (June 1, 1999): 4101–12. http://dx.doi.org/10.1128/mcb.19.6.4101.

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ABSTRACT Cryptococcus neoformans is a fungal pathogen that causes meningitis in patients immunocompromised by AIDS, chemotherapy, organ transplantation, or high-dose steroids. Current antifungal drug therapies are limited and suffer from toxic side effects and drug resistance. Here, we defined the targets and mechanisms of antifungal action of the immunosuppressant rapamycin in C. neoformans. In the yeast Saccharomyces cerevisiae and in T cells, rapamycin forms complexes with the FKBP12 prolyl isomerase that block cell cycle progression by inhibiting the TOR kinases. We identified the gene encoding a C. neoformans TOR1 homolog. Using a novel two-hybrid screen for rapamycin-dependent TOR-binding proteins, we identified the C. neoformans FKBP12 homolog, encoded by theFRR1 gene. Disruption of the FKBP12 gene conferred rapamycin and FK506 resistance but had no effect on growth, differentiation, or virulence of C. neoformans. Two spontaneous mutations that confer rapamycin resistance alter conserved residues on TOR1 or FKBP12 that are required for FKBP12-rapamycin-TOR1 interactions or FKBP12 stability. Two other spontaneous mutations result from insertion of novel DNA sequences into the FKBP12 gene. Our observations reveal that the antifungal activities of rapamycin and FK506 are mediated via FKBP12 and TOR homologs and that a high proportion of spontaneous mutants in C. neoformans result from insertion of novel DNA sequences, and they suggest that nonimmunosuppressive rapamycin analogs have potential as antifungal agents.

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Muñoz-Muñoz, Patricia L. A., Rosa E. Mares-Alejandre, Samuel G. Meléndez-López, and Marco A. Ramos-Ibarra. "Bioinformatic Analysis of Two TOR (Target of Rapamycin)-Like Proteins Encoded by Entamoeba histolytica Revealed Structural Similarities with Functional Homologs." Genes 12, no. 8 (July 28, 2021): 1139. http://dx.doi.org/10.3390/genes12081139.

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The target of rapamycin (TOR), also known as FKBP-rapamycin associated protein (FRAP), is a protein kinase belonging to the PIKK (phosphatidylinositol 3-kinase (PI3K)-related kinases) family. TOR kinases are involved in several signaling pathways that control cell growth and proliferation. Entamoeba histolytica, the protozoan parasite that causes human amoebiasis, contains two genes encoding TOR-like proteins: EhFRAP and EhTOR2. To assess their potential as drug targets to control the cell proliferation of E. histolytica, we studied the structural features of EhFRAP and EhTOR2 using a biocomputational approach. The overall results confirmed that both TOR amoebic homologs share structural similarities with functional TOR kinases, and show inherent abilities to form TORC complexes and participate in protein-protein interaction networks. To our knowledge, this study represents the first in silico characterization of the structure-function relationships of EhFRAP and EhTOR2.

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Weisman, Ronit, Irina Roitburg, Miriam Schonbrun, Rona Harari, and Martin Kupiec. "Opposite Effects of Tor1 and Tor2 on Nitrogen Starvation Responses in Fission Yeast." Genetics 175, no. 3 (December 18, 2006): 1153–62. http://dx.doi.org/10.1534/genetics.106.064170.

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Lemaire, Olivier N., Flora A. Honoré, Cécile Jourlin-Castelli, Vincent Méjean, Michel Fons, and Chantal Iobbi-Nivol. "Efficient respiration on TMAO requires TorD and TorE auxiliary proteins in Shewanella oneidensis." Research in Microbiology 167, no. 8 (October 2016): 630–37. http://dx.doi.org/10.1016/j.resmic.2016.05.004.

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Ilbert, Marianne, Vincent Méjean, Marie-Thérèse Giudici-Orticoni, Jean-Pierre Samama, and Chantal Iobbi-Nivol. "Involvement of a Mate Chaperone (TorD) in the Maturation Pathway of Molybdoenzyme TorA." Journal of Biological Chemistry 278, no. 31 (May 23, 2003): 28787–92. http://dx.doi.org/10.1074/jbc.m302730200.

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Gon, S., C. Jourlin-Castelli, L. Theraulaz, and V. Mejean. "An unsuspected autoregulatory pathway involving apocytochrome TorC and sensor TorS in Escherichia coli." Proceedings of the National Academy of Sciences 98, no. 20 (September 18, 2001): 11615–20. http://dx.doi.org/10.1073/pnas.211330598.

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Lemaire, Olivier N., Flora A. Honoré, Cécile Jourlin-Castelli, Vincent Méjean, Michel Fons, and Chantal Iobbi-Nivol. "Efficient respiration on TMAO requires TorD and TorE auxiliary proteins in Shewanella oneidensis." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1857 (August 2016): e89. http://dx.doi.org/10.1016/j.bbabio.2016.04.291.

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Martinez Marshall, Maria Nieves, Anita Emmerstorfer-Augustin, Kristin L. Leskoske, Lydia H. Zhang, Biyun Li, and Jeremy Thorner. "Analysis of the roles of phosphatidylinositol-4,5-bisphosphate and individual subunits in assembly, localization, and function of Saccharomyces cerevisiae target of rapamycin complex 2." Molecular Biology of the Cell 30, no. 12 (June 1, 2019): 1555–74. http://dx.doi.org/10.1091/mbc.e18-10-0682.

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Eukaryotic cell survival requires maintenance of plasma membrane (PM) homeostasis in response to environmental insults and changes in lipid metabolism. In yeast, a key regulator of PM homeostasis is target of rapamycin (TOR) complex 2 (TORC2), a multiprotein complex containing the evolutionarily conserved TOR protein kinase isoform Tor2. PM localization is essential for TORC2 function. One core TORC2 subunit (Avo1) and two TORC2-associated regulators (Slm1 and Slm2) contain pleckstrin homology (PH) domains that exhibit specificity for binding phosphatidylinositol-4,5- bisphosphate (PtdIns4,5P2). To investigate the roles of PtdIns4,5P2 and constituent subunits of TORC2, we used auxin-inducible degradation to systematically eliminate these factors and then examined localization, association, and function of the remaining TORC2 components. We found that PtdIns4,5P2 depletion significantly reduced TORC2 activity, yet did not prevent PM localization or cause disassembly of TORC2. Moreover, truncated Avo1 (lacking its C-terminal PH domain) was still recruited to the PM and supported growth. Even when all three PH-containing proteins were absent, the remaining TORC2 subunits were PM-bound. Revealingly, Avo3 localized to the PM independent of both Avo1 and Tor2, whereas both Tor2 and Avo1 required Avo3 for their PM anchoring. Our findings provide new mechanistic information about TORC2 and pinpoint Avo3 as pivotal for TORC2 PM localization and assembly in vivo.

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Chen, Yu-Ting, Chia-Ying Lin, Pei-Wen Tsai, Cheng-Yao Yang, Wen-Ping Hsieh, and Chung-Yu Lan. "Rhb1 Regulates the Expression of Secreted Aspartic Protease 2 through the TOR Signaling Pathway in Candida albicans." Eukaryotic Cell 11, no. 2 (December 22, 2011): 168–82. http://dx.doi.org/10.1128/ec.05200-11.

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ABSTRACTCandida albicansis a major fungal pathogen in humans. InC. albicans, secreted aspartyl protease 2 (Sap2) is the most highly expressed secreted aspartic proteasein vitroand is a virulence factor. Recent research links the small GTPase Rhb1 toC. albicanstarget of rapamycin (TOR) signaling in response to nitrogen availability. The results of this study show that Rhb1 is related to cell growth through the control ofSAP2expression when protein is the major nitrogen source. This process involves various components of the TOR signaling pathway, including Tor1 kinase and its downstream effectors. TOR signaling not only controlsSAP2transcription but also affects Sap2 protein levels, possibly through general amino acid control. DNA microarray analysis identifies other target genes downstream of Rhb1 in addition toSAP2. These findings provide new insight into nutrients, Rhb1-TOR signaling, and expression ofC. albicansvirulence factor.

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Hamed, G. R., and S. Hiza. "Trouser Tearing of a Model Natural Rubber Tire Belt Vulcanizate. Part 2: A Brief Note on the Effect of Cure Time." Rubber Chemistry and Technology 83, no. 2 (June 1, 2010): 213–15. http://dx.doi.org/10.5254/1.3548275.

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Abstract The effect of test rate on the tearing of a model natural rubber tire belt vulcanizate was previously discussed. We now discuss specimens of the same vulcanizate, cured for various times at 160 °C, which were torn apart. Prior to reversion, tear strength was high and knotty, but specimens tore rather easily when they were cured longer than the time for the onset of reversion.

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Barczak, Arkadiusz. "Podtorze jako regulator w układzie pojazd szynowy-tor." Rail Vehicles, no. 2 (April 2, 2005): 7–15. http://dx.doi.org/10.53502/rail-139796.

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W artykule przeprowadzono badania modelu układu pojazd-tor, przyjmując, że między wektorem wyjścia, którego składowe stanowią siły działające w elementach zawieszenia pojazdu, a wektorem wejścia, którego składowe stanowią przemieszczenia wynikające z nierówności toru, występuje sprzężenie zwrotne. Zatem w modelu oddziaływań między pojazdem a torem wprowadzono układ typu regulator.

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Ikai, Nobuyasu, Norihiko Nakazawa, Takeshi Hayashi, and Mitsuhiro Yanagida. "The reverse, but coordinated, roles of Tor2 (TORC1) and Tor1 (TORC2) kinases for growth, cell cycle and separase-mediated mitosis in Schizosaccharomyces pombe." Open Biology 1, no. 3 (November 2011): 110007. http://dx.doi.org/10.1098/rsob.110007.

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Target of rapamycin complexes (TORCs), which are vital for nutrient utilization, contain a catalytic subunit with the phosphatidyl inositol kinase-related kinase (PIKK) motif. TORC1 is required for cell growth, while the functions of TORC2 are less well understood. We show here that the fission yeast Schizosaccharomyces pombe TORC2 has a cell cycle role through determining the proper timing of Cdc2 Tyr15 dephosphorylation and the cell size under limited glucose, whereas TORC1 restrains mitosis and opposes securin–separase, which are essential for chromosome segregation. These results were obtained using the previously isolated TORC1 mutant tor2-L2048S in the phosphatidyl inositol kinase (PIK) domain and a new TORC2 mutant tor1-L2045D , which harbours a mutation in the same site. While mutated TORC1 and TORC2 displayed diminished kinase activity and FKBP12/Fkh1-dependent rapamycin sensitivity, their phenotypes were nearly opposite in mitosis. Premature mitosis and the G2–M delay occurred in TORC1 and TORC2 mutants, respectively. Surprisingly, separase/cut1—securin/cut2 mutants were rescued by TORC1/ tor2-L2048S mutation or rapamycin addition or even Fkh1 deletion, whereas these mutants showed synthetic defect with TORC2/ tor1-L2045D . TORC1 and TORC2 coordinate growth, mitosis and cell size control, such as Wee1 and Cdc25 do for the entry into mitosis.

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Ebell, Mark H., Akke Vellinga, Siobhan Masterson, and Phillip Yun. "Meta-analysis of the accuracy of termination of resuscitation rules for out-of-hospital cardiac arrest." Emergency Medicine Journal 36, no. 8 (May 29, 2019): 479–84. http://dx.doi.org/10.1136/emermed-2018-207833.

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BackgroundOur objective was to perform a systematic review of studies reporting the accuracy of termination of resuscitation rules (TORRs) for out-of-hospital cardiac arrest (OHCA).MethodsWe performed a comprehensive search of the literature for studies evaluating the accuracy of TORRs, with two investigators abstracting relevant data from each study regarding study design, study quality and the accuracy of the TORRs. Bivariate meta-analysis was performed using the mada procedure in R.ResultsWe identified 14 studies reporting the performance of 9 separate TORRs. The sensitivity (proportion of eventual survivors for whom the TORR recommends resuscitation and transport) was generally high: 95% for the European Resuscitation Council (ERC) TORR, 97% for the basic life support (BLS) TORR and 99% for the advanced life support (ALS) TORR. The BLS and ERC TORR were more specific, which would lead to fewer futile transports, and all three of these TORRs had a miss rate of ≤0.13% (defined as a case where a patient is recommended for termination but survives). The pooled proportion of patients for whom each rule recommends TOR was much higher for the ERC and BLS TORRs (93.5% and 74.8%, respectively) than for the ALS TORR (29.0%).ConclusionsThe BLS and ERC TORRs identify a large proportion of patients who are candidates for termination of resuscitation following OHCA while having a very low rate of misclassifying eventual survivors (<0.1%). Further prospective validation of the ERC TORR and direct comparison with BLS TORR are needed.

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Branscomb, Aron, Jon Seger, and Raymond L. White. "Evolution of Odorant Receptors Expressed in Mammalian Testes." Genetics 156, no. 2 (October 1, 2000): 785–97. http://dx.doi.org/10.1093/genetics/156.2.785.

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Abstract About 10% of mammalian odorant receptors are transcribed in testes, and odorant-receptor proteins have been detected on mature spermatozoa. Testis-expressed odorant receptors (TORs) are hypothesized to play roles in sperm chemotaxis, but they might also be ordinary nasal odorant receptors (NORs) that are expressed gratuitously in testes. Under the sperm-chemotaxis hypothesis, TORs should be subject to intense sexual selection and therefore should show higher rates of amino acid substitution than NORs, but under the gratuitous-expression hypothesis, TORs are misidentified NORs and therefore should evolve like other NORs. To test these predictions, we estimated synonymous and nonsynonymous divergences of orthologous NOR and TOR coding sequences from rat and mouse. Contrary to both hypotheses, TORs are on average more highly conserved than NORs, especially in certain domains of the OR protein. This pattern suggests that some TORs might perform internal nonolfactory functions in testes; for example, they might participate in the regulation of sperm development. However, the pattern is also consistent with a modified gratuitous-expression model in which NORs with specialized ligand specificities are both more highly conserved than typical NORs and more likely to be expressed in testes.

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Loewith, Robbie. "A brief history of TOR." Biochemical Society Transactions 39, no. 2 (March 22, 2011): 437–42. http://dx.doi.org/10.1042/bst0390437.

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The TOR (target of rapamycin) serine/threonine kinases are fascinating in that they influence many different aspects of eukaryote physiology including processes often dysregulated in disease. Beginning with the initial characterization of rapamycin as an antifungal agent, studies with yeast have contributed greatly to our understanding of the molecular pathways in which TORs operate. Recently, building on advances in quantitative MS, the rapamycin-dependent phosphoproteome in the budding yeast Saccharomyces cerevisiae was elucidated. These studies emphasize the central importance of TOR and highlight its many previously unrecognized functions. One of these, the regulation of intermediary metabolism, is discussed.

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Montella-Manuel, Sandra, Nuria Pujol-Carrion, Mónica A. Mechoud, and Maria Angeles de la Torre-Ruiz. "Bulk autophagy induction and life extension is achieved when iron is the only limited nutrient in Saccharomyces cerevisiae." Biochemical Journal 478, no. 4 (February 24, 2021): 811–37. http://dx.doi.org/10.1042/bcj20200849.

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We have investigated the effects that iron limitation provokes in Saccharomyces cerevisiae exponential cultures. We have demonstrated that one primary response is the induction of bulk autophagy mediated by TORC1. Coherently, Atg13 became dephosphorylated whereas Atg1 appeared phosphorylated. The signal of iron deprivation requires Tor2/Ypk1 activity and the inactivation of Tor1 leading to Atg13 dephosphorylation, thus triggering the autophagy process. Iron replenishment in its turn, reduces autophagy flux through the AMPK Snf1 and the subsequent activity of the iron-responsive transcription factor, Aft1. This signalling converges in Atg13 phosphorylation mediated by Tor1. Iron limitation promotes accumulation of trehalose and the increase in stress resistance leading to a quiescent state in cells. All these effects contribute to the extension of the chronological life, in a manner totally dependent on autophagy activation.

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Bageshwar, Umesh K., Antara DattaGupta, and Siegfried M. Musser. "Influence of the TorD signal peptide chaperone on Tat-dependent protein translocation." PLOS ONE 16, no. 9 (September 9, 2021): e0256715. http://dx.doi.org/10.1371/journal.pone.0256715.

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The twin-arginine translocation (Tat) pathway transports folded proteins across energetic membranes. Numerous Tat substrates contain co-factors that are inserted before transport with the assistance of redox enzyme maturation proteins (REMPs), which bind to the signal peptide of precursor proteins. How signal peptides are transferred from a REMP to a binding site on the Tat receptor complex remains unknown. Since the signal peptide mediates both interactions, possibilities include: i) a coordinated hand-off mechanism; or ii) a diffusional search after REMP dissociation. We investigated the binding interaction between substrates containing the TorA signal peptide (spTorA) and its cognate REMP, TorD, and the effect of TorD on the in vitro transport of such substrates. We found that Escherichia coli TorD is predominantly a monomer at low micromolar concentrations (dimerization KD > 50 μM), and this monomer binds reversibly to spTorA (KD ≈ 1 μM). While TorD binds to membranes (KD ≈ 100 nM), it has no apparent affinity for Tat translocons and it inhibits binding of a precursor substrate to the membrane. TorD has a minimal effect on substrate transport by the Tat system, being mildly inhibitory at high concentrations. These data are consistent with a model in which the REMP-bound signal peptide is shielded from recognition by the Tat translocon, and spontaneous dissociation of the REMP allows the substrate to engage the Tat machinery. Thus, the REMP does not assist with targeting to the Tat translocon, but rather temporarily shields the signal peptide.

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Journal articles on the topic 'Torz'

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