The core autophagy protein ATG9A controls dynamics of cell protrusions and directed migration.
Actins
/ metabolism
Autophagy
Autophagy-Related Proteins
/ metabolism
Cell Adhesion
Cell Line, Tumor
Cell Movement
Cell Surface Extensions
/ metabolism
Chemotaxis
Exocytosis
Green Fluorescent Proteins
Humans
Integrin beta1
/ metabolism
Membrane Glycoproteins
/ metabolism
Membrane Proteins
/ metabolism
Pseudopodia
/ metabolism
Reproducibility of Results
Vesicular Transport Proteins
/ metabolism
Journal
The Journal of cell biology
ISSN: 1540-8140
Titre abrégé: J Cell Biol
Pays: United States
ID NLM: 0375356
Informations de publication
Date de publication:
07 03 2022
07 03 2022
Historique:
received:
02
06
2021
revised:
09
11
2021
accepted:
08
12
2021
entrez:
18
2
2022
pubmed:
19
2
2022
medline:
3
3
2022
Statut:
ppublish
Résumé
Chemotactic migration is a fundamental cellular behavior relying on the coordinated flux of lipids and cargo proteins toward the leading edge. We found here that the core autophagy protein ATG9A plays a critical role in the chemotactic migration of several human cell lines, including highly invasive glioma cells. Depletion of ATG9A protein altered the formation of large and persistent filamentous actin (F-actin)-rich lamellipodia that normally drive directional migration. Using live-cell TIRF microscopy, we demonstrated that ATG9A-positive vesicles are targeted toward the migration front of polarized cells, where their exocytosis correlates with protrusive activity. Finally, we found that ATG9A was critical for efficient delivery of β1 integrin to the leading edge and normal adhesion dynamics. Collectively, our data uncover a new function for ATG9A protein and indicate that ATG9A-positive vesicles are mobilized during chemotactic stimulation to facilitate expansion of the lamellipodium and its anchorage to the extracellular matrix.
Identifiants
pubmed: 35180289
pii: 213022
doi: 10.1083/jcb.202106014
pmc: PMC8932524
pii:
doi:
Substances chimiques
Actins
0
ATG9A protein, human
0
Autophagy-Related Proteins
0
Integrin beta1
0
Membrane Glycoproteins
0
Membrane Proteins
0
PHluorin
0
TGOLN2 protein, human
0
Vesicular Transport Proteins
0
Green Fluorescent Proteins
147336-22-9
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2022 Campisi et al.
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