MTC7 is predicted to encode a small, poorly characterized Saccharomyces cerevisiae membrane protein with two predicted transmembrane helices and a basic, disordered C-terminal region. Genetic-screen data linked MTC7 to cdc13-1 modifier phenotypes and led to the maintenance of telomere capping 7 name, but the evidence does not establish a direct role for Mtc7 in chromosome-end capping. The protein product, molecular activity, direct partners, precise compartment of action, and mechanistic relationship to telomere biology remain unverified.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0016020 membrane | IEA GO_REF:0000120 | ACCEPT | Summary: UniProt annotates Mtc7 as a predicted multi-pass membrane protein, and the sequence contains two predicted transmembrane helices. This is currently the only supported cellular-component annotation in GOA. Reason: The membrane annotation is appropriately broad and is supported by sequence-based transmembrane prediction in UniProt, but protein existence is PE 4 (Predicted), and no stronger compartment-specific experimental localization was found in the current GOA/UniProt-derived files. No Huh et al. GFP-library compartment call is represented for MTC7 here. Supporting Evidence: UniProt:P32633 SUBCELLULAR LOCATION: Membrane; Multi-pass membrane protein. TRANSMEM features are annotated at residues 13-33 and 42-62. file:yeast/MTC7/MTC7-bioinformatics/RESULTS.md The Kyte-Doolittle scan generated by tm_analysis_results.json predicted one segment, residues 45-63, which overlaps UniProt's second TRANSMEM feature but did not independently recover TM1. |
| GO:0003674 molecular_function | ND GO_REF:0000015 | ACCEPT | Summary: The ND molecular-function annotation remains appropriate. MTC7 has no demonstrated enzymatic, binding, transporter, or adaptor activity in the accessible literature or Falcon report. Reason: Mtc7 is genetically associated with telomere-capping phenotypes, but no molecular function has been measured. SGD retained this ND annotation in 2013, after both the 2004 telomere-length screen and the 2008 cdc13-1 modifier screen; retaining the ND annotation is more defensible than inferring DNA binding, protein binding, or a telomere structural role. Supporting Evidence: file:yeast/MTC7/MTC7-deep-research-falcon.md No study in the retrieved corpus provides a direct molecular function for Mtc7 (no catalytic reaction, substrate specificity, binding activity, or domain assignment). |
| GO:0005575 cellular_component | ND GO_REF:0000015 | ACCEPT | Summary: Root cellular component ND annotation: when it was made, no cellular component had been curated for this gene product from literature. Reason: ACCEPT under the ND acceptance rule (projects/NO_DATA.md). The evidence this review cites for the cellular component is inferred (from orthologs, family membership or sequence features) or comes from other species; none of it is literature on this gene product in this species. This was judged from the review's own content during the NO_DATA re-action pass, not from a new literature search. Earlier action: REMOVE. The literature-search record in MTC7-deep-research-falcon.md finds no study of this S. cerevisiae gene product that identifies a cellular location. Supporting Evidence: file:yeast/MTC7/MTC7-deep-research-falcon.md No primary localization evidence for Mtc7/YEL033W was retrieved. |
| GO:0008150 biological_process | ND GO_REF:0000015 | ACCEPT | Summary: The generic ND biological-process placeholder remains appropriate because MTC7 has no experimentally established biological process. Reason: Addinall et al. named MTC7 from a cdc13-1 genome-wide genetic interaction screen, but that high-throughput phenotype does not show that Mtc7 itself carries out chromosome-end capping, acts in the CST complex, or even acts at telomeres. An earlier genome-wide telomere-length screen explicitly found that the YEL033W short-telomere phenotype failed to cosegregate with the deletion marker. Telomere biology remains a hypothesis for targeted follow-up, not a demonstrated process annotation; SGD likewise left MTC7 at biological_process ND in 2013. Supporting Evidence: PMID:18845848 We also identified a number of genes of previously unknown function that we term RTC, for restriction of telomere capping, or MTC, for maintenance of telomere capping. PMID:15161972 The single exception, yel033w , showed a short telomere phenotype that segregated independently from the antibiotic resistance. |
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Download this section (compressed HTML)Q: What molecular activity does Mtc7 carry out, and does it bind a specific telomere-associated protein, membrane complex, RNA, or DNA substrate?
Q: Is Mtc7 physically present at telomeres, at an endomembrane compartment, or does it influence telomere capping indirectly through chromatin or stress response pathways?
Q: Which phenotype of mtc7 deletion is primary: defective telomere capping, altered telomere length maintenance, or a broader membrane-linked stress response that modifies cdc13-1 viability?
Experiment: Measure telomere length, single-stranded telomeric DNA accumulation, and checkpoint activation in mtc7 deletion cells and mtc7 cdc13-1 double mutants across permissive and semi-permissive temperatures.
Type: genetics
Experiment: Determine Mtc7 localization using endogenously tagged, functional Mtc7 combined with membrane markers and telomere-marker ChIP or live-cell imaging assays.
Type: microscopy
Experiment: Identify Mtc7 physical interactors by affinity purification-mass spectrometry under normal and telomere-uncapping stress conditions, followed by validation of candidates from telomere, chromatin, and membrane pathways.
Type: proteomics
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Download this section (compressed HTML)Protein of unknown function; predicted metabolic role based on network analysis derived from ChIP experiments, a large-scale deletion study and localization of transcription factor binding sites; null mutant is sensitive to temperature oscillation in a cdc13-1 mutant
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Download this section (compressed HTML)📊 View Pathway Visualization Interactive pathway diagram with detailed annotations