Oliver's mTOR Atlas Evidence Platform
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Pathway link MTORC1-NUCL

mTORC1 Nucleotide synthesis

mTORC1 activates Nucleotide synthesis.

mTORC1 turns on the machinery for building DNA/RNA building blocks, so a growing cell can actually copy its DNA.

mTORC1 couples nucleotide supply to demand - it turns on purine synthesis through the mitochondrial tetrahydrofolate cycle so a dividing cell can actually copy its DNA.

The conditions it holds under

Cancer cell and mammalian cell studies, including xenograft tumours (VAL2017, BEN2016, ALI2022). The evidence comes mostly from dividing or tumour cells; whether non-dividing tissues use the same route is not shown.

Time it takes
hours
Step
indirect (through steps not drawn here)
Measured in
mammalian cells
Where in the cell
cytosol
Reaches people?
plausible in people, not shown directly
How settled
settled in the literature

Studies behind it

YearEvidenceStudy
2017 M mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic VulnerabilityVAL2017 Hyperactive mTORC1 couples nucleotide synthesis to demand; imbalance drives replication stress in these cells.
2016 M mTORC1 induces purine synthesis through control of the mitochondrial tetrahydrofolate cycleBEN2016 mTORC1 promotes purine synthesis via ATF4-driven mitochondrial tetrahydrofolate metabolism.
2022 M The mTORC1-SLC4A7 axis stimulates bicarbonate import to enhance de novo nucleotide synthesisALI2022 Building a nucleotide needs a carbon donor, and cells get it from bicarbonate dissolved in their surroundings. This study shows mTORC1 does not just switch on the nucleotide enzymes - it also arranges the delivery of the raw material. Through S6K and the translation factor eIF4B, mTORC1 selectively increases translation of the mRNA for SLC4A7, a sodium-bicarbonate cotransporter, so more bicarbonate is pulled into the cell. Removing SLC4A7 from cells with hyperactive mTORC1 cut flux through both de novo purine and pyrimidine synthesis and slowed cell and tumor growth, without changing intracellular pH - so the transporter matters as a supply line, not as a pH regulator. A fourth distinct route by which mTORC1 feeds nucleotide synthesis, alongside CAD (BEN2013), the mitochondrial folate cycle (BEN2016) and demand coupling (VAL2017).

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.

“How settled” describes how far researchers in the field agree. It is not the same as the sign-off above, which only says whether a named curator has checked this page.

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