The TORC1 signaling pathway plays a major role in the control of cell growth and response to stress. Here we demonstrate that the SEA complex physically interacts with TORC1 and is an important regulator of its activity. During nitrogen starvation, deletions of SEA complex components lead to Tor1 kinase delocalization, defects in autophagy, and vacuolar fragmentation. TORC1 inactivation, via nitrogen deprivation or rapamycin treatment, changes cellular levels of SEA complex members. We used affinity purification and chemical cross-linking to generate the data for an integrative structure modeling approach, which produced a well-defined molecular architecture of the SEA complex and showed that the SEA complex comprises two regions that are structurally and functionally distinct. The SEA complex emerges as a platform that can coordinate both structural and enzymatic activities necessary for the effective functioning of the TORC1 pathway.
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| Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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| Gene | Phenotype | Experiment Type | Mutant Information | Strain Background | Chemical | Details |
|---|---|---|---|---|---|---|
| IML1 | autophagy: decreased | classical genetics | null Allele: iml1-Δ | Other | Media: nitrogen starvation Details: autophagic induction and flux are decreased; monitored by the maturation and localization of autophagy marker GFP-Atg8 | |
| RTC1 | protein/peptide accumulation: increased Reporter: Npr3p-GFP | classical genetics | null Allele: rtc1-Δ | Other | sirolimus | Details: Npr3p is stabilized in cells treated with rapamycin |
| MTC5 | protein/peptide accumulation: increased Reporter: Npr3p-GFP | classical genetics | null Allele: mtc5-Δ | Other | sirolimus | Details: Npr3p is stabilized in cells treated with rapamycin |
| SEA4 | protein/peptide accumulation: increased Reporter: Npr3p-GFP | classical genetics | null Allele: sea4-Δ | Other | sirolimus | Details: Npr3p is stabilized in cells treated with rapamycin |
| IML1 | protein/peptide accumulation: increased Reporter: Npr3p-GFP | classical genetics | null Allele: iml1-Δ | Other | sirolimus | Details: Npr3p is stabilized in cells treated with rapamycin |
| NPR2 | protein/peptide distribution: abnormal Reporter: Tor1p-GFP | classical genetics | null Allele: npr2-Δ | Other | Media: nitrogen starvation Details: Tor1p becomes dispersed in cytoplasmic foci after 20 hrs of nitrogen starvation, rather than remain in the vacuolar membrane | |
| NPR3 | protein/peptide distribution: abnormal Reporter: Tor1p-GFP | classical genetics | null Allele: npr3-Δ | Other | Media: nitrogen starvation Details: Tor1p becomes dispersed in cytoplasmic foci after 20 hrs of nitrogen starvation, rather than remain in the vacuolar membrane | |
| IML1 | protein/peptide distribution: abnormal Reporter: Tor1p-GFP | classical genetics | null Allele: iml1-Δ | Other | Media: nitrogen starvation Details: Tor1p becomes dispersed in cytoplasmic foci after 20 hrs of nitrogen starvation, rather than remain in the vacuolar membrane | |
| IML1 | vacuolar morphology: abnormal | classical genetics | null Allele: iml1-Δ | Other | Media: nitrogen starvation Details: significant vacuolar fragmentation; vacuolar fusion is inhibited |
Increase the total number of rows showing on this page by using the pull-down located below the table, or use the page scroll at the table's top right to browse through the table's pages; use the arrows to the right of a column header to sort by that column; filter the table using the "Filter" box at the top of the table; click on the small "i" buttons located within a cell for an annotation to view further details about experiment type and any other genes involved in the interaction.
| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Increase the total number of rows showing on this page by using the pull-down located below the table, or use the page scroll at the table's top right to browse through the table's pages; use the arrows to the right of a column header to sort by that column; filter the table using the "Filter" box at the top of the table; click on the small "i" buttons located within a cell for an annotation to view further details about experiment type and any other genes involved in the interaction.
| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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