Pathway link MTORC1-RIBOBIO
mTORC1 Ribosome biogenesis
mTORC1 activates Ribosome biogenesis.
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.
The conditions it 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.
- Time it takes
- hours
- Step
- indirect (through steps not drawn here)
- Measured in
- budding yeast, human cells
- Where in the cell
- nucleus
- Reaches people?
- plausible in people, not shown directly
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2022 | M | TORC1 and PKA activity towards ribosome biogenesis oscillates in synchrony with the budding yeast cell cycleGUE2022 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 metastasisHSI2012 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. |
| 2026 | M | mTOR inactivation governs adaptive survival to ribosome biogenesis deficiencyFAN2026 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. |
Points the other way
No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.
Who has checked this
- Checked by
- No researcher outside the project has checked this link yet.
- Curator sign-off
- Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
- Curated by
- Oliver Barton, with AI help for drafting; see how links are checked.
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