AIP limits neurotransmitter release by inhibiting calcium bursts from the ryanodine receptor

Bojun Chen, Ping Liu, Edward J. Hujber, Yan Li, Erik M. Jorgensen and Zhao-Wen Wang ()
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Bojun Chen: University of Connecticut Health Center
Ping Liu: University of Connecticut Health Center
Edward J. Hujber: University of Utah
Yan Li: University of Connecticut Health Center
Erik M. Jorgensen: University of Utah
Zhao-Wen Wang: University of Connecticut Health Center

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract Pituitary tumors are frequently associated with mutations in the AIP gene and are sometimes associated with hypersecretion of growth hormone. It is unclear whether other factors besides an enlarged pituitary contribute to the hypersecretion. In a genetic screen for suppressors of reduced neurotransmitter release, we identified a mutation in Caenorhabditis elegans AIPR-1 (AIP-related-1), which causes profound increases in evoked and spontaneous neurotransmitter release, a high frequency of spontaneous calcium transients in motor neurons and an enlarged readily releasable pool of vesicles. Calcium bursts and hypersecretion are reversed by mutations in the ryanodine receptor but not in the voltage-gated calcium channel, indicating that these phenotypes are caused by a leaky ryanodine receptor. AIPR-1 is physically associated with the ryanodine receptor at synapses. Finally, the phenotypes in aipr-1 mutants can be rescued by presynaptic expression of mouse AIP, demonstrating that a conserved function of AIP proteins is to inhibit calcium release from ryanodine receptors.

Date: 2017
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DOI: 10.1038/s41467-017-01704-z

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