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Publication : The AP-2 complex interacts with γ-TuRC and regulates the proliferative capacity of neural progenitors.

First Author  Camblor-Perujo S Year  2024
Journal  Life Sci Alliance Volume  7
Issue  2 PubMed ID  38086550
Mgi Jnum  J:343451 Mgi Id  MGI:7566717
Doi  10.26508/lsa.202302029 Citation  Camblor-Perujo S, et al. (2024) The AP-2 complex interacts with gamma-TuRC and regulates the proliferative capacity of neural progenitors. Life Sci Alliance 7(2)
abstractText  Centrosomes are organelles that nucleate microtubules via the activity of gamma-tubulin ring complexes (gamma-TuRC). In the developing brain, centrosome integrity is central to the progression of the neural progenitor cell cycle, and its loss leads to microcephaly. We show that NPCs maintain centrosome integrity via the endocytic adaptor protein complex-2 (AP-2). NPCs lacking AP-2 exhibit defects in centrosome formation and mitotic progression, accompanied by DNA damage and accumulation of p53. This function of AP-2 in regulating the proliferative capacity of NPCs is independent of its role in clathrin-mediated endocytosis and is coupled to its association with the GCP2, GCP3, and GCP4 components of gamma-TuRC. We find that AP-2 maintains gamma-TuRC organization and regulates centrosome function at the level of MT nucleation. Taken together, our data reveal a novel, noncanonical function of AP-2 in regulating the proliferative capacity of NPCs and open new avenues for the identification of novel therapeutic strategies for the treatment of neurodevelopmental and neurodegenerative disorders with AP-2 complex dysfunction.
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