Proteomics

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Transcriptional regulation of ER-phagy by MiT/TFE factors controls chondrocyte differentiation and bone formation

ABSTRACT: Lysosomal-autophagic degradation of Endoplasmic Reticulum via autophagy (ER-phagy) is emerging as critical regulator of ER homeostasis and function. However, the molecular mechanisms governing ER-phagy are still unknown. Working in chondrocytes, we found that ER-phagy and lysosome biogenesis are co-activated by FGF signaling during hypertrophic differentiation, a mandatory step for bone formation. FGF induced ER-phagy trough IRS1-dependent inhibition of the insulin signaling and activation of MiT/TFE transcription factors, master regulators of lysosome biogenesis. MiT/TFE promoted ER-phagy through the induction of the ER-phagy receptor FAM134B. Notably, the activation of ER-phagy promotes chondrocytes differentiation and secretion of factors required for cartilage replacement by bone. Consistently, medaka fish knock-down for FAM134B have impaired ossification of cranial bones. Thus, ER-phagy is a transcriptionally regulated process that participates to cell differentiation during development.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Rattus Norvegicus (rat)

SUBMITTER: Natalie Krahmer  

LAB HEAD: Carmine Settembre

PROVIDER: PXD015331 | Pride | 2020-07-15

REPOSITORIES: Pride

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Publications

Lysosomal degradation of the endoplasmic reticulum (ER) via autophagy (ER-phagy) is emerging as a critical regulator of cell homeostasis and function. The recent identification of ER-phagy receptors has shed light on the molecular mechanisms underlining this process. However, the signaling pathways regulating ER-phagy in response to cellular needs are still largely unknown. We found that the nutrient responsive transcription factors TFEB and TFE3-master regulators of lysosomal biogenesis and aut  ...[more]

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