Oliver's mTOR Atlas Evidence Platform
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Pathway link MTORC2-ACTIN

mTORC2 Actin cytoskeleton

mTORC2 activates Actin cytoskeleton.

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.

One of the first functions assigned to mTORC2 was shaping the cell's skeleton. In yeast it was the original TOR2 phenotype; in mammalian cells it showed that the second complex is acutely rapamycin-insensitive.

The conditions 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.

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

Studies behind it

YearEvidenceStudy
2004 M Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitiveJAC2004 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 cytoskeletonSAR2004 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 controlLOE2002 Defined two distinct TOR complexes, only one rapamycin-sensitive, founding the TORC1/TORC2 paradigm.
2013 A mTORC2 controls actin polymerization required for consolidation of long-term memoryHUA2013 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.

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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