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TFEB controls Retromer expression in response to nutrient availability

Research output: Contribution to journalArticle

Original languageEnglish
JournalJournal of Cell Biology
DateAccepted/In press - 23 Sep 2019


Endosomal recycling maintains the cell surface abundance of nutrient transporters for nutrient uptake but how the cell integrates nutrient availability with recycling is less well understood. Here, in studying the recycling of human glutamine transporters ASCT2 (SLC1A5), LAT1 (SLC7A5), SNAT1 (SLC38A1) and SNAT2 (SLC38A2) we establish that following amino acid restriction the adaptive delivery of SNAT2 to the cell surface relies on Retromer, a master conductor of endosomal recycling. Upon complete amino acid starvation or selective glutamine depletion, we establish that Retromer expression is upregulated by TFEB (transcription factor EB) and other members of the MiTF/TFE family of transcription factors through association with CLEAR elements in the promoters of the Retromer genes VPS35 and VPS26A. TFEB regulation of Retromer expression therefore supports adaptive nutrient acquisition through endosomal recycling.



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