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The Autophagy Regulator p62 Controls PTEN-Dependent Ciliogenesis
Hyowon Mun1, Eun Ji Lee1, Minah Park1
1Department of Biological Science, Sookmyung Women's University, Seoul, South Korea.
Frontiers in Cell and Developmental Biology
|June 27, 2020
Summary
Altering autophagy, a cellular recycling process, inhibits cilia assembly. This effect is mediated by the autophagy regulator p62 through the Pten/Dvl2/AurKA signaling pathway, revealing a link between nutrient sensing and cilia formation.
Area of Science:
- Cell Biology
- Molecular Biology
- Organelle Biology
Background:
- Autophagy is a crucial catabolic process for maintaining cellular energy balance and recycling macromolecules.
- It functions as a nutrient-sensing mechanism, typically suppressed when nutrients are abundant and induced during starvation.
- Cilia are energy-sensing organelles involved in cellular signaling, also responsive to nutrient deprivation.
Purpose of the Study:
- To investigate the impact of altered autophagy on cilia assembly.
- To elucidate the specific molecular mechanisms underlying the relationship between autophagy and ciliogenesis.
Main Methods:
- Modulation of autophagy flux using pharmacological inhibitors and small interfering RNAs (siRNAs).
- Assessment of cilia assembly and ciliogenesis.
- Analysis of the involvement of the autophagy regulator p62 and the Pten/Dvl2/AurKA signaling pathway.
Main Results:
- Disrupting autophagy flux, through chemical or genetic means, significantly inhibited ciliogenesis.
- The observed inhibition of cilia assembly was dependent on the autophagy regulator p62.
- The mechanism involved the Pten/Dvl2/AurKA signaling pathway, linking autophagy status to cilia formation.
Conclusions:
- Autophagy plays a critical role in regulating cilia assembly.
- The p62-mediated regulation of Pten/Dvl2/AurKA signaling is a key mechanism connecting autophagy and ciliogenesis.
- These findings highlight a novel interplay between cellular catabolism and organelle biogenesis in response to nutrient availability.
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