| Autor: |
Ji-Hye Kwak, You-kyung Lee, Mi-Hee Jun, Mootaek Roh, Hyunhyo Seo, Juhyun Lee, Kyungmin Lee, Jin-A Lee |
| Jazyk: |
angličtina |
| Rok vydání: |
2021 |
| Předmět: |
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| Zdroj: |
Molecular Brain, Vol 14, Iss 1, Pp 1-5 (2021) |
| Druh dokumentu: |
article |
| ISSN: |
1756-6606 |
| DOI: |
10.1186/s13041-021-00814-6 |
| Popis: |
Abstract Autophagy is a lysosomal degradation pathway that regulates cellular homeostasis. It is constitutively active in neurons and controls the essential steps of neuronal development, leading to its dysfunction in neurodevelopmental disorders. Although mTOR-associated impaired autophagy has previously been reported in neurodevelopmental disorders, there is lack of information about the dysregulation of mTOR-independent autophagy in neurodevelopmental disorders. In this study, we investigated whether the loss of Epac2, involved in the mTOR-independent pathway, affects autophagy activity and whether the activity of autophagy is associated with social–behavioral phenotypes in mice with Epac2 deficiencies. We observed an accumulation of autophagosomes and a significant increase in autophagic flux in Epac2-deficient neurons, which had no effect on mTOR activity. Next, we examined whether an increase in autophagic activity contributed to the social behavior exhibited in Epac2 −/− mice. The social recognition deficit observed in Epac2 −/− mice recovered in double transgenic Epac2 −/− : Atg5 +/− mice. Our study suggests that excessive autophagy due to Epac2 deficiencies may contribute to social recognition defects through an mTOR-independent pathway. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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