Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival

Efeyan A, Zoncu R, Chang S, Gumper I, Snitkin H, Wolfson RL, Kirak O, Sabatini DD, Sabatini DM · 2012 · Nature · Atlas ID EFE2012

What this study shows

Rag-GTPase control of mTORC1 is essential for neonatal autophagy and survival to fasting.

Abstract

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The mechanistic target of rapamycin complex 1 (mTORC1) pathway regulates organismal growth in response to many environmental cues, including nutrients and growth factors. Cell-based studies showed that mTORC1 senses amino acids through the RagA-D family of GTPases (also known as RRAGA, B, C and D), but their importance in mammalian physiology is unknown. Here we generate knock-in mice that express a constitutively active form of RagA (RagA(GTP)) from its endogenous promoter. RagA(GTP/GTP) mice develop normally, but fail to survive postnatal day 1.

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At a glance

Evidence type	A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (RagA GTP knock-in)); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Mouse (RagA GTP knock-in)
Journal	Nature
Year	2012
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1038/nature11745 · PMID 23263183 · Free full text (PMC4000705)

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 – constitutively active RagA(GTP) knock-in
Target	mTORC1 / Rag GTPases
Model	Mouse (RagA GTP knock-in)
Effect	Constitutive RagA→mTORC1 blocks fasting-induced autophagy in neonates → death on postnatal day 1 when fasted
Dose	not stated
Sample size	not stated
Effect size	Treatment of pups at birth with rapamycin significantly delayed the death of fasted RagA GTP/GTP neonates from ~14 h to ~21 h (p<0.01).
Limitations	not stated

In the Atlas

Links in the pathway map

Supports Rag GTPases recruits mTORC1

Cite this paper

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Efeyan, A., Zoncu, R., Chang, S., Gumper, I., Snitkin, H., Wolfson, R. L., Kirak, O., Sabatini, D. D., & Sabatini, D. M. (2012). Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival. Nature. https://doi.org/10.1038/nature11745

@article{EFE2012,
  author       = {Efeyan, A. and Zoncu, R. and Chang, S. and Gumper, I. and Snitkin, H. and Wolfson, R. L. and Kirak, O. and Sabatini, D. D. and Sabatini, D. M.},
  title        = {{Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival}},
  journal      = {Nature},
  year         = {2012},
  doi          = {10.1038/nature11745},
  note         = {PMID: 23263183},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record EFE2012) [Data set]. https://mtor-atlas.org/study/EFE2012/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_EFE2012,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record EFE2012},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/EFE2012/},
  doi          = {10.5281/zenodo.22059963}
}

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