Mechanisms of neuronal survival safeguarded by endocytosis and autophagy. Issue 2 (21st October 2020)
- Record Type:
- Journal Article
- Title:
- Mechanisms of neuronal survival safeguarded by endocytosis and autophagy. Issue 2 (21st October 2020)
- Main Title:
- Mechanisms of neuronal survival safeguarded by endocytosis and autophagy
- Authors:
- Overhoff, Melina
De Bruyckere, Elodie
Kononenko, Natalia L. - Other Names:
- Cousin Michael A. guestEditor.
Smillie Karen guestEditor.
Gordon Sarah guestEditor. - Abstract:
- Abstract: Multiple aspects of neuronal physiology crucially depend on two cellular pathways, autophagy and endocytosis. During endocytosis, extracellular components either unbound or recognized by membrane‐localized receptors (termed "cargo") become internalized into plasma membrane‐derived vesicles. These can serve to either recycle the material back to the plasma membrane or send it for degradation to lysosomes. Autophagy also uses lysosomes as a terminal degradation point, although instead of degrading the plasma membrane‐derived cargo, autophagy eliminates detrimental cytosolic material and intracellular organelles, which are transported to lysosomes by means of double‐membrane vesicles, referred to as autophagosomes. Neurons, like all non‐neuronal cells, capitalize on autophagy and endocytosis to communicate with the environment and maintain protein and organelle homeostasis. Additionally, the highly polarized, post‐mitotic nature of neurons made them adopt these two pathways for cell‐specific functions. These include the maintenance of the synaptic vesicle pool in the pre‐synaptic terminal and the long‐distance transport of signaling molecules. Originally discovered independently from each other, it is now clear that autophagy and endocytosis are closely interconnected and share several common participating molecules. Considering the crucial role of autophagy and endocytosis in cell type‐specific functions in neurons, it is not surprising that defects in both pathwaysAbstract: Multiple aspects of neuronal physiology crucially depend on two cellular pathways, autophagy and endocytosis. During endocytosis, extracellular components either unbound or recognized by membrane‐localized receptors (termed "cargo") become internalized into plasma membrane‐derived vesicles. These can serve to either recycle the material back to the plasma membrane or send it for degradation to lysosomes. Autophagy also uses lysosomes as a terminal degradation point, although instead of degrading the plasma membrane‐derived cargo, autophagy eliminates detrimental cytosolic material and intracellular organelles, which are transported to lysosomes by means of double‐membrane vesicles, referred to as autophagosomes. Neurons, like all non‐neuronal cells, capitalize on autophagy and endocytosis to communicate with the environment and maintain protein and organelle homeostasis. Additionally, the highly polarized, post‐mitotic nature of neurons made them adopt these two pathways for cell‐specific functions. These include the maintenance of the synaptic vesicle pool in the pre‐synaptic terminal and the long‐distance transport of signaling molecules. Originally discovered independently from each other, it is now clear that autophagy and endocytosis are closely interconnected and share several common participating molecules. Considering the crucial role of autophagy and endocytosis in cell type‐specific functions in neurons, it is not surprising that defects in both pathways have been linked to the pathology of numerous neurodegenerative diseases. In this review, we highlight the recent knowledge of the role of endocytosis and autophagy in neurons with a special focus on synaptic physiology and discuss how impairments in genes coding for autophagy and endocytosis proteins can cause neurodegeneration. Abstract : Multiple aspects of neuronal physiology crucially depend on two cellular pathways, autophagy, and endocytosis. Originally discovered independently from each other, it is now clear that autophagy and endocytosis are closely interconnected and share several common participating molecules. Considering the crucial role of autophagy and endocytosis in cell type‐specific functions in neurons, it is not surprising that defects in both pathways have been linked to the pathology of numerous neurodegenerative diseases. In this review, we highlight the recent knowledge of the role of endocytosis and autophagy in neurons with a special focus on synaptic physiology and discuss how impairments in genes coding for autophagy and endocytosis proteins can cause neurodegeneration. … (more)
- Is Part Of:
- Journal of neurochemistry. Volume 157:Issue 2(2021)
- Journal:
- Journal of neurochemistry
- Issue:
- Volume 157:Issue 2(2021)
- Issue Display:
- Volume 157, Issue 2 (2021)
- Year:
- 2021
- Volume:
- 157
- Issue:
- 2
- Issue Sort Value:
- 2021-0157-0002-0000
- Page Start:
- 263
- Page End:
- 296
- Publication Date:
- 2020-10-21
- Subjects:
- amphisomes -- autophagy -- endocytosis -- neurodegeneration -- protein aggregations -- synaptic vesicles
Neurochemistry -- Periodicals
616.8042 - Journal URLs:
- http://www.blackwell-synergy.com/loi/jnc ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/jnc.15194 ↗
- Languages:
- English
- ISSNs:
- 0022-3042
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5021.500000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 22608.xml