Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic Gene Ontology annotation based on Rhea mapping
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Regulation of ribosome biogenesis by the rapamycin-sensitive TOR-signaling pathway in Saccharomyces cerevisiae.
Tor proteins and protein phosphatase 2A reciprocally regulate Tap42 in controlling cell growth in yeast.
HEAT repeats mediate plasma membrane localization of Tor2p in yeast.
The TOR-controlled transcription activators GLN3, RTG1, and RTG3 are regulated in response to intracellular levels of glutamine.
Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control.
LST8 negatively regulates amino acid biosynthesis as a component of the TOR pathway.
TOR complex 1 includes a novel component, Tco89p (YPL180w), and cooperates with Ssd1p to maintain cellular integrity in Saccharomyces cerevisiae.
Proteome survey reveals modularity of the yeast cell machinery.
Global landscape of protein complexes in the yeast Saccharomyces cerevisiae.
Nutrient regulates Tor1 nuclear localization and association with rDNA promoter.
TOR signaling is a determinant of cell survival in response to DNA damage.
Hsf1 activation inhibits rapamycin resistance and TOR signaling in yeast revealed by combined proteomic and genetic analysis.
TOR1 and TOR2 have distinct locations in live cells.
Superoxide anions regulate TORC1 and its ability to bind Fpr1:rapamycin complex.
The Vam6 GEF controls TORC1 by activating the EGO complex.
A global protein kinase and phosphatase interaction network in yeast.
TORC1-regulated protein kinase Npr1 phosphorylates Orm to stimulate complex sphingolipid synthesis.
Reciprocal conversion of Gtr1 and Gtr2 nucleotide-binding states by Npr2-Npr3 inactivates TORC1 and induces autophagy.
TORC1 and TORC2 work together to regulate ribosomal protein S6 phosphorylation in Saccharomyces cerevisiae.
One library to make them all: streamlining the creation of yeast libraries via a SWAp-Tag strategy.
The TOR signaling pathway regulates starvation-induced pseudouridylation of yeast U2 snRNA.
Slm35 links mitochondrial stress response and longevity through TOR signaling pathway.
Hyperactive TORC1 sensitizes yeast cells to endoplasmic reticulum stress by compromising cell wall integrity.
TORC1 phosphorylates and inhibits the ribosome preservation factor Stm1 to activate dormant ribosomes.
Pib2 is a cysteine sensor involved in TORC1 activation in Saccharomyces cerevisiae.
TOR1 and TOR2 are structurally and functionally similar but not identical phosphatidylinositol kinase homologues in yeast.
TOR controls translation initiation and early G1 progression in yeast.
Target of rapamycin proteins and their kinase activities are required for meiosis.
Tor, a phosphatidylinositol kinase homologue, controls autophagy in yeast.
Falcon (Edison Scientific) deep research report on Saccharomyces cerevisiae TOR1 (P35169)
-
TOR1 is a large PI3/PI4-kinase-family (PIKK) atypical serine/threonine protein
kinase; its C-terminal kinase domain is the catalytically relevant region, and
the biologically relevant activity is Ser/Thr protein kinase activity rather than
lipid kinase activity, despite the historical phosphatidylinositol kinase homolog name.
"TOR1 encodes a large PI3/PI4-kinase-family, atypical serine/threonine protein kinase; its C-terminal kinase region is the catalytically relevant domain."
-
In budding yeast TOR1 is the primary catalytic subunit of the rapamycin-sensitive
TORC1 complex (Tor1/Tor2 + Kog1/RAPTOR + Lst8). tor1-delta is viable whereas
tor2-delta is lethal; TORC2 requires Tor2 exclusively, so TOR1 is a TORC1 subunit,
not a TORC2 subunit.
"tor1Δ is viable** whereas **tor2Δ is lethal**; TORC1 can function with either Tor1 or Tor2, but **TORC2 requires Tor2**"
-
TORC1 is the rapamycin-sensitive TOR complex; its core composition is Tor1 or Tor2
plus Kog1 (RAPTOR ortholog) and Lst8.
"TORC1** is the **rapamycin-sensitive** complex; its core is described as **Tor1 or Tor2 + Kog1 (RAPTOR ortholog) + Lst8**"
-
TORC1 signaling is organized at the vacuolar membrane (analogous to
lysosome-associated mTORC1), where TORC1 is recruited and regulated by Rag-family
GTPases (Gtr1-Gtr2) and the EGO complex.
"A core concept in yeast is that **TORC1 signaling is organized at the vacuolar membrane** (analogous to lysosome-associated mTORC1 in mammals). In budding yeast, TORC1 is recruited/regulated at the **vacuolar membrane** by Rag-family GTPases (**Gtr1–Gtr2**) and the **EGO complex**."
-
Upon glucose depletion or post-diauxic shift, TORC1 redistributes into inhibited
vacuolar puncta/condensates called TOROIDs (TORC1 Organized in Inhibited Domains);
a 2023 cryo-EM study (3.9 A) showed EGOC binding structurally activates TORC1 by
antagonizing TOROID polymerization.
"redistributes into vacuolar puncta/condensates called TOROIDs"
-
TORC1 is activated mainly by amino acids and nutrients through the Gtr1-Gtr2
Rag-family GTPases and the EGO complex; the active state corresponds to Gtr1-GTP
and Gtr2-GDP.
"TORC1 activity in yeast is primarily stimulated by amino acids through **Rag-family GTPases** (**Gtr1–Gtr2**)."
-
TOR1/TORC1 promotes protein synthesis, translation initiation, and ribosome
biogenesis and suppresses autophagy under nutrient-rich conditions, acting largely
through the Sch9 and Tap42 downstream branches.
"controls **protein synthesis and ribosome biogenesis**, with major downstream branches involving **Sch9** and **Tap42**"
-
Loss of TOR1/2 signaling or rapamycin treatment causes a severe reduction in
protein synthesis and triggers starvation-like physiology including autophagy
induction; TOR is a pivotal negative regulator of autophagy acting upstream of the
core autophagy machinery.
"loss of TOR1/2 signaling or rapamycin treatment causes a severe reduction in protein synthesis"
-
Reduced TOR1/TORC1 signaling causes early G1/G0 arrest, glycogen accumulation,
thermotolerance, vacuole enlargement, autophagy induction, and starvation-like
transcriptional reprogramming.
"Reduced TOR1/TORC1 signaling causes early G1/G0 arrest"
-
Dominant rapamycin-resistant TOR1 alleles map to the FRB domain, including
substitutions at Ser1972 (to Arg or Asn), pinpointing the TOR-FKBP12-rapamycin
interaction interface; rapamycin acts through FKBP12 (Fpr1 in yeast).
"Dominant TOR1 rapamycin-resistant alleles map to the **FRB domain**, including substitutions at **Ser1972 (to Arg or Asn)**, which pinpoints the TOR–FKBP12–rapamycin interaction interface."
-
Substrate-linked pathway evidence: TOR pathway activity phosphorylates the Ser/Thr
kinase Npr1; loss of TOR signaling causes rapid Npr1 dephosphorylation and
starvation-induced turnover of the tryptophan permease Tat2. TOR also promotes
association of PP2A-related phosphatases with Tap42.
"TOR pathway activity phosphorylates the Ser/Thr kinase Npr1"