Ribosome biogenesis
Making new ribosomes: rRNA transcription by RNA polymerase I, 5S and tRNA transcription by RNA polymerase III, and the translation of ribosomal-protein mRNAs. Distinct from how efficiently existing ribosomes work. Added 2026-10-10 after an audit found the Atlas had no node for it, although the 5'TOP mRNA entity already asserted that this output is canonical for mTORC1.
Building new protein factories. Building new ribosomes, the machines that make proteins. This is different from making the ribosomes a cell already has work faster. A growing cell has to do both, and mTORC1 has a say in each.
Distinct from translational efficiency. The two polymerase steps that carry most of this output are not measured by any study in this corpus: mTOR controls Pol I through TIF-IA and Pol III through Maf1, both outside the corpus, so read this node as the existence of the output rather than as its mechanism.
TL;DR. Ribosome biogenesis appears in 3 curated studies in Oliver's mTOR Atlas: 3 at the molecular level (cells, biochemistry, structure). No study in people is recorded for it in the Atlas yet. It has 1 interaction in the curated pathway model.
In the pathway model
| Interaction | Mechanism | Evidence | Studies |
|---|---|---|---|
| mTORC1 activates Ribosome biogenesis mechanism: functional-consequence · this link in full · on the map table | A growing cell needs more ribosomes, not just busier ones, and mTORC1 has a say in how many get built. That was followed through the cell cycle in yeast, and in mammalian cells the programme mTORC1 controls turns out to be dominated by the ribosome's own parts. The link runs in both directions: block ribosome building and the cell turns mTOR down to cope. TORC1 activity tracks ribosome biogenesis: in budding yeast TORC1 and PKA activity towards ribosome biogenesis oscillates with the cell cycle (GUE2022), and in mammalian cells the translational programme mTORC1 controls is dominated by the ribosome's own components (HSI2012). The dependency also runs the other way: when ribosome biogenesis fails, mTOR inactivation is what lets cells survive it (FAN2026). TORC1 activity tracks ribosome biogenesis: in budding yeast TORC1 and PKA activity towards ribosome biogenesis oscillates with the cell cycle (GUE2022), and in mammalian cells the translational programme mTORC1 controls is dominated by the ribosome's own components (HSI2012). The dependency also runs the other way: when ribosome biogenesis fails, mTOR inactivation is what lets cells survive it (FAN2026). Holds under: The two polymerase steps that carry most of this output are NOT measured by any study in this corpus. mTOR controls rRNA transcription through RNA polymerase I via TIF-IA (Mayer 2004, PMID 15004009, outside this corpus) and tRNA and 5S transcription through RNA polymerase III via Maf1 (Shor 2010, PMID 20233713, outside this corpus). Until those are curated here the edge rests on a yeast cell-cycle study, a mammalian ribosome-profiling study and a reverse-direction survival study, so read it as the existence of the output rather than as its mechanism. plausible in people, not shown directly · emerging, few independent studies | M | GUE2022, HSI2012, FAN2026 |
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| M | Molecular — cells, biochemistry, structure | 3 |
No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.
Studies
| Year | Evidence | Study |
|---|---|---|
| 2026 | M | mTOR inactivation governs adaptive survival to ribosome biogenesis deficiency FAN2026 mTORC1 inhibition does not restore ribosome biogenesis but redistributes limited ribosomes away from highly-translated 5'TOP mRNAs toward survival-essential transcripts, defining a 'translational fitness' mechanism that lets cancer cells survive ribosome biogenesis deficiency. |
| 2022 | M | TORC1 and PKA activity towards ribosome biogenesis oscillates in synchrony with the budding yeast cell cycle GUE2022 Tracking the localisation of two TORC1 and PKA targets by time-lapse microscopy in hundreds of yeast cells shows that TORC1/PKA activity towards ribosome biogenesis rises and falls in step with the cell cycle even when outside conditions stay constant; mutations in upstream regulators suggest internal metabolic signals partly drive the oscillation. |
| 2012 | M | The translational landscape of mTOR signalling steers cancer initiation and metastasis HSI2012 Showed WHY mTOR-driven translation matters for cancer: in prostate cancer, oncogenic mTOR selectively translates a specific set of pro-invasion mRNAs that drive metastasis. An ATP-competitive mTOR inhibitor (INK128) reversed that signature - an early preclinical rationale from mouse models and cell lines, not a clinical result. |
Related entities
Thank you. Your answer was counted anonymously.