Illustration of LC3 proteins relocating to damaged Golgi apparatus, symbolizing cellular repair.

Is Your Golgi Apparatus Trying to Tell You Something? The Surprising Link Between Cellular Stress and LC3 Recruitment

Nico Varela in Science & Nature July 2025 • 4 min read.

"New research reveals how your cells respond to damage, offering insights into autophagy and potential therapeutic strategies."

In the bustling metropolis of your cells, every organelle has a job. Among them, the Golgi apparatus, a kind of cellular post office, processes and packages proteins for delivery throughout the cell. But what happens when this critical organelle gets damaged? New research is shedding light on a surprising cellular response, one that could have major implications for our understanding of cell health and disease.

A recent study published in Cell Death & Differentiation unveils a novel mechanism by which cells respond to damage in the Golgi apparatus. Researchers discovered that when the Golgi is compromised, cells recruit a protein called LC3 to the site of the injury. LC3 is best known for its role in autophagy, a cellular self-cleaning process that removes damaged components. This discovery suggests a previously unknown link between Golgi damage and the autophagy pathway.

But what does this mean for you? Understanding how cells respond to stress and damage at a fundamental level can open doors to new therapeutic strategies for a range of conditions. From neurodegenerative diseases to cancer, the ability to manipulate cellular responses could revolutionize how we approach treatment.

LC3: Not Just for Autophagy—A First Responder to Golgi Damage?

Illustration of LC3 proteins relocating to damaged Golgi apparatus, symbolizing cellular repair.

LC3, or microtubule-associated protein 1A/1B-light chain 3, is a key player in autophagy. Typically, LC3 is found diffusely in the cell's cytoplasm, but when autophagy is triggered, it concentrates at the membranes of autophagosomes, the structures that engulf damaged cell parts for recycling. However, this new research indicates LC3 has a broader role.

The study demonstrated that when the Golgi apparatus is damaged—whether by lasers, specific chemical compounds, or other stressors—LC3 relocates to the Golgi. This recruitment doesn't necessarily lead to the formation of autophagosomes. Instead, LC3 appears to be involved in a different kind of response, one that scientists are still working to fully understand.

Here’s what the researchers uncovered:

Damage Signals LC3: Various methods of Golgi damage, including laser-induced damage and certain drugs, all triggered LC3 recruitment.
ATG5 is Essential: The protein ATG5, crucial for autophagy, is also required for LC3 to move to the damaged Golgi.
No Double Membrane: Unlike typical autophagy, this process doesn't involve the formation of double-membraned autophagosomes.
Cellular Protection: When cells couldn't recruit LC3 (due to a lack of ATG5), they were more prone to cell death, suggesting this pathway is protective.

This targeted relocation of LC3 suggests that it serves a cytoprotective function, potentially preventing cell death by helping to repair or manage the damage. The researchers found that cells unable to recruit LC3 to the Golgi were more vulnerable to cell death when the Golgi was stressed. This suggests that LC3 is part of a defense mechanism, ensuring cell survival when under attack.

What Does This Mean for the Future?

This research opens fascinating new avenues for understanding and treating diseases linked to cellular stress and organelle dysfunction. By identifying the key molecules involved in LC3 recruitment to the Golgi, scientists can develop targeted therapies to enhance this protective pathway. This could potentially slow the progression of neurodegenerative diseases, improve cancer treatment outcomes, and promote healthy aging by bolstering the cell's natural defense mechanisms.

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This article is based on research published under:

DOI-LINK: 10.1038/s41418-018-0221-5, Alternate LINK

Title: Recruitment Of Lc3 To Damaged Golgi Apparatus

Subject: Cell Biology

Journal: Cell Death & Differentiation

Publisher: Springer Science and Business Media LLC

Authors: Lígia C. Gomes-Da-Silva, Ana Joaquina Jimenez, Allan Sauvat, Wei Xie, Sylvie Souquere, Séverine Divoux, Marko Storch, Baldur Sveinbjørnsson, Øystein Rekdal, Luis G. Arnaut, Oliver Kepp, Guido Kroemer, Franck Perez

Published: 2018-10-22

Everything You Need To Know

What is the main function of the Golgi apparatus within a cell?

The Golgi apparatus functions as a cellular 'post office'. It processes and packages proteins for delivery to various locations within the cell. When the Golgi apparatus is compromised, cells recruit LC3 to the site of the injury.

How does LC3 normally function in a healthy cell, and how does its role change when the Golgi apparatus is damaged?

Typically, LC3 (microtubule-associated protein 1A/1B-light chain 3) is involved in autophagy, a process where damaged cell parts are engulfed by autophagosomes for recycling. When the Golgi apparatus is damaged, LC3 relocates to the Golgi. However, this recruitment doesn't necessarily lead to the formation of autophagosomes. Instead, LC3 appears to be involved in a different kind of response, one that scientists are still working to fully understand.

What role does ATG5 play in the recruitment of LC3 to the damaged Golgi apparatus?

ATG5 is essential for LC3 to move to the damaged Golgi apparatus. Without ATG5, LC3 cannot be recruited to the Golgi when it's under stress. Researchers found that cells unable to recruit LC3 to the Golgi were more vulnerable to cell death when the Golgi was stressed.

In what ways is the LC3 response to Golgi damage different from its role in typical autophagy?

Unlike typical autophagy, the recruitment of LC3 to the Golgi apparatus doesn't involve the formation of double-membraned autophagosomes. Instead, LC3 appears to be involved in a different kind of response that scientists are still working to fully understand. This targeted relocation of LC3 suggests that it serves a cytoprotective function, potentially preventing cell death by helping to repair or manage the damage.

What are the potential therapeutic implications of understanding how cells recruit LC3 to the damaged Golgi apparatus, particularly in diseases like cancer or neurodegenerative disorders?

By identifying the key molecules involved in LC3 recruitment to the Golgi, scientists can develop targeted therapies to enhance this protective pathway. This could potentially slow the progression of neurodegenerative diseases, improve cancer treatment outcomes, and promote healthy aging by bolstering the cell's natural defense mechanisms. In cancer, for instance, enhancing LC3 recruitment could make cancer cells more vulnerable to treatments that induce cellular stress. For neurodegenerative diseases, boosting this pathway could help cells better manage and repair damage, potentially slowing disease progression.