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Autophagy

Autophagy

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.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...

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Related Experiment Video

Updated: Aug 22, 2025

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Published on: October 18, 2024

Epitranscriptomic turbo for autophagy boost: m⁶A reader YTHDF3.

WeiChao Hao^1,2, MeiJuan Dian^3,4, JiaHong Wang²

¹Department of Oncology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.

|November 14, 2022

Summary

Nutrient starvation triggers autophagy via the m6A reader YTHDF3. This protein enhances autophagosome formation and lysosomal function by promoting FOXO3 translation, linking epitranscriptomics to cellular homeostasis.

Keywords:

Autophagy FOXO3 METTL3 YTHDF3 epitranscriptomics m6A nutrient starvation

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Last Updated: Aug 22, 2025

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

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Published on: June 12, 2017

Area of Science:

Cell Biology
Molecular Biology
Epigenetics

Background:

Autophagy is crucial for cellular homeostasis, particularly during nutrient starvation.
The role of epitranscriptomic modifications in autophagy remains largely unexplored.
N6-methyladenosine (m6A) is a key epitranscriptomic mark.

Purpose of the Study:

To investigate the involvement of epitranscriptomic events in autophagy induction.
To elucidate the role of the m6A reader YTHDF3 in nutrient starvation-induced autophagy.

Main Methods:

Investigated the function of YTHDF3 in autophagy.
Analyzed m6A modifications on Foxo3 mRNA.
Examined the recruitment of translation factors EIF3A and EIF4B.
Assessed autophagosome formation and lysosomal function.

Main Results:

YTHDF3 is essential for autophagy induction during nutrient deficiency.
Elevated m6A levels, installed by METTL3, enhance YTHDF3's function.
YTHDF3 binds to m6A sites on Foxo3 mRNA (CDS and 3' UTR near stop codon).
This binding promotes FOXO3 translation via EIF3A and EIF4B recruitment, boosting autophagy.

Conclusions:

YTHDF3 acts as a critical sensor of nutrient starvation, linking m6A epitranscriptomic modifications to autophagy.
The YTHDF3-mediated promotion of FOXO3 translation is a key mechanism for upregulating autophagy.
Findings provide insights into how RNA post-transcriptional modifications regulate nutrient-sensing pathways and cellular recycling.