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MAP6 interacts with Tctex1 and Ca v 2.2/N‐type calcium channels to regulate calcium signalling in neurons
Author(s) -
Brocard Jacques,
Dufour Fabrice,
GoryFauré Sylvie,
Arnoult Christophe,
Bosc Christophe,
Denarier Eric,
Peris Leticia,
Saoudi Yasmina,
De Waard Michel,
Andrieux Annie
Publication year - 2017
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13766
Subject(s) - calcium , microbiology and biotechnology , calcium signaling , p type calcium channel , signalling , t type calcium channel , voltage dependent calcium channel , biology , neuroscience , dynein , microtubule , calcium binding protein , chemistry , signal transduction , organic chemistry
Abstract MAP6 proteins were first described as microtubule‐stabilizing agents, whose properties were thought to be essential for neuronal development and maintenance of complex neuronal networks. However, deletion of all MAP6 isoforms in MAP6 KO mice does not lead to dramatic morphological aberrations of the brain but rather to alterations in multiple neurotransmissions and severe behavioural impairments. A search for protein partners of MAP6 proteins identified Tctex1 – a dynein light chain with multiple non‐microtubule‐related functions. The involvement of Tctex1 in calcium signalling led to investigate it in MAP6 KO neurons. In this study, we show that functional Ca v 2.2/N‐type calcium channels are deficient in MAP6 KO neurons, due to improper location. We also show that MAP6 proteins interact directly with both Tctex1 and the C‐terminus of Ca v 2.2/N‐type calcium channels. A balance of these two interactions seems to be crucial for MAP6 to modulate calcium signalling in neurons.