PTEN regulates microtubule polymerization via mTORC2, but not mTORC1, in peripheral sensory neurons
What this study shows
Uses Raptor (mTORC1) versus Rictor (mTORC2) co-deletion on a Pten-knockout background to ask which complex carries the growth signal to the microtubule cytoskeleton. Suppressing mTORC2 — but not mTORC1 — returns the accelerated microtubule polymerisation and neuronal hypertrophy of Pten-KO neurons to wild-type levels, and the effect is confined to the axonal growth cone rather than the proximal axon shaft. A clean genetic dissection on the comparatively thin mTORC2 side of the pathway.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Mouse peripheral sensory neuron cultures (Pten-KO with Raptor or Rictor co-deletion, both sexes)) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Mouse peripheral sensory neuron cultures (Pten-KO with Raptor or Rictor co-deletion, both sexes) |
| Journal | eNeuro |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1523/ENEURO.0116-26.2026 · PMID 42642329 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Genetic: Pten knockout with Raptor (mTORC1) or Rictor (mTORC2) co-deletion |
| Target | mTORC2 (RICTOR); microtubule cytoskeleton; PTEN |
| Model | Mouse (peripheral sensory neuron cultures) |
| Effect | mTORC2, not mTORC1, mediates PTEN-dependent microtubule polymerization and neuronal hypertrophy at the growth cone |
In the Atlas
Related topics
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- Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1 (2006)
- mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice (2009)
- mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways (2004)
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