期刊
CELLS
卷 11, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/cells11050842
关键词
hippocampus; calcium; ER-mitochondria contact sites; neuron
类别
资金
- Ministerio de Ciencia, Innovacion y Universidades [RTI2018-094678-A-I00, RTI2018-094374-B-I00]
This study explores the function of Pyk2 in mitochondria-associated membranes (MAMs) and demonstrates its role in regulating ER-mitochondria calcium efflux, affecting mitochondrial function and leading to calcium homeostasis imbalance.
Pyk2 is a non-receptor tyrosine kinase enriched in hippocampal neurons, which can be activated by calcium-dependent mechanisms. In neurons, Pyk2 is mostly localised in the cytosol and dendritic shafts but can translocate to spines and/or to the nucleus. Here, we explore the function of a new localisation of Pyk2 in mitochondria-associated membranes (MAMs), a subdomain of ER-mitochondria surface that acts as a signalling hub in calcium regulation. To test the role of Pyk2 in MAMs' calcium transport, we used full Pyk2 knockout mice (Pyk2(-/-)) for in vivo and in vitro studies. Here we report that Pyk2(-/-) hippocampal neurons present increased ER-mitochondrial contacts along with defective calcium homeostasis. We also show how the absence of Pyk2 modulates mitochondrial dynamics and morphology. Taken all together, our results point out that Pyk2 could be highly relevant in the modulation of ER-mitochondria calcium efflux, affecting in turn mitochondrial function.
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