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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Selective autophagy bears bone.

Milana Fraiberg1, Zvulun Elazar1

  • 1Department of Biomolecular Sciences, The Weizmann Institute of Science, Rehovot, Israel.

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Fibroblast growth factor 18 (FGF18) activates endoplasmic reticulum selective autophagy (ER-phagy) by regulating the Fam134b receptor. This process is crucial for maintaining ER proteostasis and skeletal development.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Autophagy Research

Background:

  • The endoplasmic reticulum (ER) is vital for protein folding and maturation.
  • Selective autophagy of the ER (ER-phagy) is an emerging process for maintaining ER proteostasis.
  • ER-phagy is regulated by cellular growth conditions.

Discussion:

  • Cinque et al. (2020) demonstrate that fibroblast growth factor 18 (FGF18) specifically induces ER-phagy.
  • This induction is mediated by TFEB/TFE-dependent transcriptional regulation of the ER-phagy receptor Fam134b.
  • The study highlights the role of FGF18 in ER homeostasis and its implications for bone development.

Key Insights:

  • FGF18 acts as a specific activator of ER-phagy.
  • TFEB/TFE transcription factors are key regulators in the FGF18-mediated ER-phagy pathway.
  • Fam134b is a critical ER-phagy receptor regulated by FGF18 signaling.

Outlook:

  • Further research into the FGF18-Fam134b axis could reveal new therapeutic targets for skeletal disorders.
  • Understanding ER-phagy regulation by growth factors may offer insights into broader cellular stress responses.
  • Investigating the precise mechanisms linking ER-phagy to bone ossification is warranted.