IP3 receptor isoforms differently regulate ER-mitochondrial contacts and local calcium transfer

Adam Bartok, David Weaver, Tünde Golenár, Zuzana Nichtova, Máté Katona, Száva Bánsághi, Kamil J. Alzayady, V. Kaye Thomas, Hideaki Ando, Katsuhiko Mikoshiba, Suresh K. Joseph, David I. Yule, György Csordás () and György Hajnóczky ()
Additional contact information
Adam Bartok: Thomas Jefferson University
David Weaver: Thomas Jefferson University
Tünde Golenár: Thomas Jefferson University
Zuzana Nichtova: Thomas Jefferson University
Máté Katona: Thomas Jefferson University
Száva Bánsághi: Thomas Jefferson University
Kamil J. Alzayady: University of Rochester
V. Kaye Thomas: University of Rochester
Hideaki Ando: RIKEN Brain Science Institute
Katsuhiko Mikoshiba: RIKEN Brain Science Institute
Suresh K. Joseph: Thomas Jefferson University
David I. Yule: University of Rochester
György Csordás: Thomas Jefferson University
György Hajnóczky: Thomas Jefferson University

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Contact sites of endoplasmic reticulum (ER) and mitochondria locally convey calcium signals between the IP3 receptors (IP3R) and the mitochondrial calcium uniporter, and are central to cell survival. It remains unclear whether IP3Rs also have a structural role in contact formation and whether the different IP3R isoforms have redundant functions. Using an IP3R-deficient cell model rescued with each of the three IP3R isoforms and an array of super-resolution and ultrastructural approaches we demonstrate that IP3Rs are required for maintaining ER-mitochondrial contacts. This role is independent of calcium fluxes. We also show that, while each isoform can support contacts, type 2 IP3R is the most effective in delivering calcium to the mitochondria. Thus, these studies reveal a non-canonical, structural role for the IP3Rs and direct attention towards the type 2 IP3R that was previously neglected in the context of ER-mitochondrial calcium signaling.

Date: 2019
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DOI: 10.1038/s41467-019-11646-3

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