Organellar Ca²⁺ Transport in Plant versus Animal Cells: Can We Learn from Each Other?

Dear Colleagues,

Ca²⁺ is the second primary messenger inside cells and acts as the most prominent signal in many biological processes in plant and animal cells. In addition to Ca²⁺ influx and efflux across the plasma membrane, intracellular organelles also participate in concert to orchestrate Ca²⁺ dynamics that control cellular functions locally and globally. The relevance of intracellular organelle Ca²⁺ transporters in regulating cell function has been recognized for a very long time. The recent advancements in applying genetic, chemical and super-resolution imaging tools have placed the research of organellar Ca²⁺ transporters at the center stage over the last decade.

Nevertheless, the important topic covered in this Special Issue is yet to be discussed systematically. This Special Issue aims to collect original manuscripts and review articles on recent findings of organellar Ca²⁺ transport studies in plant and animal cells, with an attempt to shed light on the fundamental principles that govern their commonalities and differences throughout the evolution. As such, we may learn from this comparison and to further advance this research field.

Prof. Dr. Shey-Shing Sheu
Prof. Dr. Marc Freichel
Guest Editors

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• organellar calcium transport
• plant cells
• animal cells
• intracellular organelle communication
• calcium signaling
• mitochondria
• organelle-targeted florescent Ca²⁺ indicators
• super-resolution imaging

Title: Sarcoplasmic reticulum-mitochondria contacts: impact on cardiac physiology and mitochondrial fitness
Authors: Sergio De la Fuente1, 2, *, Shey-Shing Sheu1, ǂ, Celia Fernandez-Sanz1, *, ǂ
Affiliation: 1 Center for Translational Medicine, Department of Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 19107 USA. 2 Instituto de Biología y Genética Molecular (IBGM), Departamento de Bioquímica y Biología Molecular y Fi-siología, Facultad de Medicina, Universidad de Valladolid and Consejo Superior de Investigaciones Cientí-ficas (CSIC), Ramon y Cajal, 7, E-47005 Valladolid, Spain.

Title: MIRO1 is required for dynamic increases in mitochondria ER contact sites and mitochondrial ATP during the cell cycle
Authors: Isabella M. Grumbach; Benney T. Endoni; Olha M. Koval; Chantal Allamargot; Tara Kortlever; Lan Qian; Riley J. Sadoski; Denise Juhr
Affiliation: Abboud Cardiovascular Research Center, Division of Cardiovascular Medicine, Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City IA 52242, USA.
Abstract: Mitochondria ER contact sites (MERCS) are vital for mitochondrial dynamics, lipid exchange, Ca2+ homeostasis, and energy metabolism. We examined whether mitochondrial metabolism changes during the cell cycle depend on MERCS dynamics and are regulated by outer mitochondrial rho GTPase 1 (MIRO1). Wound healing was assessed in mice with fibroblast-specific deletion of MIRO1. Wild-type and MIRO1-/- fibroblasts and vascular smooth muscle cells were evaluated for proliferation, cell cycle progression, MERCS number, distance, and protein composition throughout the cell cycle. Restoration of MIRO1 mutants tested the role of MIRO1 domains; Ca2+ transients and mitochondrial metabolism were evaluated using biochemical, immunodetection, and fluorescence techniques. MERCS increased in number during G1/S compared to G0, accompanied by a notable rise in protein-protein interactions involving VDAC1 and IP3R, as well as GRP75 and MIRO1 by proximity-ligation assays. Split GFP ER/mitochondrial contacts of 40 nm also increased. Mitochondrial [Ca2+], membrane potential, and ATP levels correlated with MERCS formation during the cell cycle. MIRO1 deficiency blocked G1/S progression and the cell cycle-dependent formation of MERCS, and altered ER Ca2+ release and mitochondrial Ca2+ uptake. MIRO1 mutants lacking the Ca2+-sensitive EF hands or the transmembrane domain did not rescue cell proliferation or MERCS formation. MIRO1 controls an increase in the number of MERCS during cell- cycle progression and increases mitochondrial [Ca2+], driving metabolic activity and proliferation through its EF hands.