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Atlastins remodel the endoplasmic reticulum for selective autophagy.

Jin Rui LiangEmily LingemanSaba AhmedJacob E Corn
Published in: The Journal of cell biology (2018)
Specific receptors are required for the autophagic degradation of endoplasmic reticulum (ER), known as ER-phagy. However, little is known about how the ER is remodeled and separated for packaging into autophagosomes. We developed two ER-phagy-specific reporter systems and found that Atlastins are key positive effectors and also targets of ER-phagy. Atlastins are ER-resident GTPases involved in ER membrane morphology, and Atlastin-depleted cells have decreased ER-phagy under starvation conditions. Atlastin's role in ER-phagy requires a functional GTPase domain and proper ER localization, both of which are also involved in ER architecture. The three Atlastin family members functionally compensate for one another during ER-phagy and may form heteromeric complexes with one another. We further find that Atlastins act downstream of the FAM134B ER-phagy receptor, such that depletion of Atlastins represses ER-autophagy induced by the overexpression of FAM134B. We propose that during ER-phagy, Atlastins remodel ER membrane to separate pieces of FAM134B-marked ER for efficient autophagosomal engulfment.
Keyphrases
  • endoplasmic reticulum
  • estrogen receptor
  • breast cancer cells
  • cell death
  • cell proliferation
  • endoplasmic reticulum stress
  • transcription factor
  • signaling pathway
  • patient safety
  • induced apoptosis
  • crispr cas
  • pi k akt