Actin cytoskeleton
Cell shape and motility machinery. The original TOR2 phenotype in yeast, and the mammalian mTORC2 function that showed the second complex is acutely rapamycin-insensitive (JAC2004, SAR2004); the two-complex model itself came from biochemistry (LOE2002).
The cell's internal scaffolding. The scaffolding that gives a cell its shape and lets it move. It was one of the first jobs pinned on mTORC2 - first in yeast, then in mammalian cells - and one that rapamycin does not block in the short term. The idea of two separate mTOR complexes itself came from purifying the proteins.
The original TORC2 phenotype in yeast; in mammals mediated through PKCα and Rho GTPases and largely rapamycin-insensitive acutely.
TL;DR. Actin cytoskeleton appears in 4 curated studies in Oliver's mTOR Atlas: 1 in animal models; 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 |
|---|---|---|---|
| mTORC2 activates Actin cytoskeleton mechanism: functional-consequence · this link in full · on the map table | mTORC2's first known job was shaping the cell's internal skeleton. It was found in yeast first, as the original TOR2 phenotype, and then in mammalian cells - where it stood out precisely because rapamycin didn't block it. Holds under: Mammalian cells, yeast, Drosophila and conditional Rictor-knockout mice (JAC2004, SAR2004, LOE2002, HUA2013). The cytoskeleton phenotype was defined in cell lines and yeast; its role in intact tissue is less tested. plausible in people, not shown directly · settled in the literature | A | JAC2004, SAR2004, LOE2002, HUA2013 |
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| A | Animal model | 1 |
| 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 |
|---|---|---|
| 2013 | A | mTORC2 controls actin polymerization required for consolidation of long-term memory HUA2013 Conditional deletion of Rictor in the postnatal mouse forebrain reduced mTORC2 activity and selectively impaired long-term memory and the late phase of hippocampal LTP, with a comparable long-term-memory deficit in dTORC2-deficient flies. Hippocampal actin polymerisation was reduced, and restoring it rescued both L-LTP and long-term memory; a compound that raised mTORC2 activity converted early LTP into late LTP and enhanced memory. This is the loss-of-function AND rescue evidence that mTORC2 is required for memory consolidation - the arm chronic rapamycin also disrupts, and the study Open Question H8 needs for its mTORC2 liability leg, which until 2026-09-05 rested on no supporting study at all. |
| 2004 | M | Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive JAC2004 mTORC2 (rictor) controls the actin cytoskeleton and is rapamycin-insensitive, defining a second mTOR complex in mammals. |
| 2004 | M | Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton SAR2004 Discovery of Rictor and the SECOND mTOR complex, mTORC2. Crucially showed this complex is NOT blocked by rapamycin and does not use Raptor - it controls the cytoskeleton via PKC. This is the paper that split mTOR biology into 'two faces' at the molecular level. |
| 2002 | M | Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control LOE2002 Defined two distinct TOR complexes, only one rapamycin-sensitive, founding the TORC1/TORC2 paradigm. |
Related entities
Thank you. Your answer was counted anonymously.