Oliver's mTOR Atlas Evidence Platform
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Shawn M. Ferguson

Showed mTORC1 directly phosphorylates TFEB to keep the cell's lysosome-building program switched off

BS/MS, Univ. of Ottawa · PhD Neuroscience, Vanderbilt · postdoc, Yale (Pietro De Camilli) · now Professor of Cell Biology and Neuroscience, Yale School of Medicine

Ferguson Lab, Yale School of Medicine ↗

Shawn M. Ferguson Portrait: Yale School of Medicine

Showed (ROC2012) mTORC1 phosphorylates TFEB (Ser211), recruiting 14-3-3 to trap it in the cytoplasm — independent, complementary work to the Settembre/Ballabio TFEB papers. Follow-up (PET2013): folliculin (FLCN, a Birt-Hogg-Dubé tumor suppressor) is recruited to lysosomes by amino acids, binding RagA to support mTORC1 activation.

Trained in neuroscience before shifting to lysosome cell biology with De Camilli at Yale; now studies lysosomal adaptation and neurodegenerative disease (Parkinson's, ALS, FTD, Alzheimer's).

Milestones in the Atlas

YearEvidenceStudy
2012 M The transcription factor TFEB links mTORC1 signaling to transcriptional control of lysosome homeostasis ROC2012 mTORC1 phosphorylates TFEB to keep it cytoplasmically sequestered via 14-3-3.
2013 M Recruitment of folliculin to lysosomes supports the amino acid-dependent activation of Rag GTPases PET2013 Amino acids recruit folliculin (FLCN) to lysosomes to support Rag-dependent mTORC1 activation.

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