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Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
Published on: February 18, 2014
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Atlastins remodel the endoplasmic reticulum for selective autophagy
Jin Rui Liang1,2, Emily Lingeman1,2, Saba Ahmed1,2
1Innovative Genomics Institute, University of California, Berkeley, Berkeley, CA.
The Journal of Cell Biology
|August 26, 2018
Summary
Atlastins, ER-resident GTPases, are crucial for endoplasmic reticulum (ER) degradation via ER-phagy. They remodel ER membranes, enabling efficient autophagosome packaging of ER components marked by the FAM134B receptor.
Area of Science:
- Cellular Biology
- Molecular Biology
- Autophagy Research
Background:
- Endoplasmic reticulum (ER) degradation through autophagy, termed ER-phagy, requires specific receptors.
- Mechanisms of ER remodeling and segregation for autophagosomal packaging remain largely unknown.
Purpose of the Study:
- To investigate the role of ER-resident GTPases, specifically Atlastins, in the process of ER-phagy.
- To elucidate how ER membrane morphology is regulated during ER-phagy.
Main Methods:
- Development of two novel ER-phagy-specific reporter systems.
- Depletion studies of Atlastin family members and the FAM134B receptor.
- Analysis of Atlastin's GTPase domain and ER localization.
Main Results:
- Atlastins were identified as key positive effectors and targets of ER-phagy.
- Atlastin-depleted cells exhibited significantly reduced ER-phagy levels, particularly under starvation conditions.
- Atlastin's function in ER-phagy depends on its GTPase activity and ER localization, which are integral to ER architecture.
- The three Atlastin family members showed functional redundancy and potential for heteromeric complex formation.
- Atlastins function downstream of the FAM134B receptor, with Atlastin depletion inhibiting FAM134B-induced ER-autophagy.
Conclusions:
- Atlastins play a critical role in remodeling ER membranes to facilitate their segregation and engulfment by autophagosomes during ER-phagy.
- These findings reveal a novel mechanism for ER membrane remodeling essential for selective autophagy.
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