MAP6 interacts with Tctex1 and Cav2.2/N-type calcium channels to regulate calcium signaling in neurons

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 behavioral 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 signaling led to investigate it in MAP6 KO neurons. In the present study, we show that functional Ca_v2.2/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_v2.2/N-type calcium channels. A balance of these two interactions seems to be crucial for MAP6 to modulate calcium signaling in neurons.

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