Topics

ECI - Early Career Investigator

Ast Tslil

Weizmann Institute of Science, Rehovot, IL

ECI: Ironing out protein synthesis: METTL17 is an Fe-S cluster checkpoint for mitochondrial translation

Djurabekova Amina

Department of Physics, University of Helsinki, FI-00014, Helsinki, FI

ECI: Analysis of the Atomistic MD Simulations of CI+CIII Interactions and Associated Lipid Binding.

Esparza-Perusquia Mercedes

National Autonomous University of Mexico, MX

ECI: What we have learned about the dimeric complex V, and what it could still teach us.

Hofmann Julia

Department of Visceral, Transplant and Thoracic Surgery, organLife, Medical University of Innsbruck, AT

ECI: Fueling success: Harnessing liver bioenergetics in clinical- and long-term machine perfusion.

Jones Scott

University of Cambridge, UK

ECI: Nucleotide specificity of human uncoupling protein 1 inhibition.

Mazza Tiziano

University of Calabria, IT

ECI: Unveiling the Modulation of MRP2 Activity: Insights from Phosphorylation and Drug Interactions.

Merono Luca

University of Freiburg, DE

ECI: The role of a quinol anion in respiratory complex I

Mohammed Sami

University of Veterinary Medicine, Vienna, AT

ECI: Mutational analysis of the mammalian mitochondrial Ca²⁺/H⁺ exchanger TMBIM5/MICS1

Pfleger Ana

University of Innsbruck, AT

ECI:

Rodriguez Enrique

University College London Genetics, Evolution and Environment, London, UK

ECI: Subtle changes in respiratory function produce big differences in life-history traits in stressed mitonuclear fly lines.

Scherr Margareta

University of Innsbruck, AT

ECI: From Childhood Trauma to immunocellular health: Unveiling the Link between Adverse Experiences and Depression

Sichrovsky Maximilian

University of Cambridge, UK

ECI: Identification of the Inhibitor Binding Site of the Human Mitochondrial Pyruvate Carrier.

Strich Sophie

Institute of Molecular Biology, University of Innsbruck / Tyrolean Cancer Research Institute (TKFI), AT

ECI: Mitochondrial bioenergetic profiling reveals off-target effects of kinase inhibitors in cancer cell models.

Zdorevskyi Oleksii

Department of Physics, University of Helsinki, FI-00014, Helsinki, FI

ECI: Long-range charge transfer in respiratory complex I: an insight from multi-scale molecular dynamics simulations.

1. From quantum physics and quantum information chemistry to quantum biology of respiratory and photosynthetic electron transfer. 80 years after Erwin Schrödinger's What is Life?

Goodson Theodore III

Executive Editor, Journal of Physical Chemistry
Department of Chemistry, University of Michigan, US

I would enjoy giving a talk about both the findings of the committee [ref 1] and my own research in quantum coherence in organic and biological systems.

Lane Nick

Department of Genetics, Evolution and Environment, University College London, UK

I’ve been doing a little work on anaesthetics and mitochondria in relation to quantum biology – maybe I will talk about that at EBEC2024.

Sharma Vivek

HiLife Institute of Biotechnology, University of Helsinki, Biocenter, Viikinkaari; Department of Physics, University of Helsinki, Gustaf Hällströmin katu, Helsinki, FI

Mechanistic insights on respiratory complexes and supercomplexes using multiscale computer simulations.

I will talk about our recent work on respiratory complexes and supercomplexes and how biomolecular dynamics of membrane, protein and solvent water plays a critical role in catalysis, all studied by molecular dynamics simulations and quantum chemistry applied on high-resolution structural data.

2. Protonmotive force, long-range electron transfer, magnetic fields, and thermodynamic and kinetic control of bioenergetics

Kell Douglas

Research Chair in Systems Biology, Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Biosciences Building, University of Liverpool, Liverpool, UK

A protet-based model for oxidative and photosynthetic phosphorylation.

Sheu Shey-Shing

Center for Translational Medicine, Department of Medicine, Center for Mitochondrial Imaging Research and Diagnostics (MitoCare), Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, US

Low Magnetic Fields Stimulate Cardiac Mitochondrial Bioenergetics, Possibly Through the Radical Pair Mechanism.

3. Evolution and bioenergetics

Allen John

Research Department of Genetics, Evolution and Environment, University College London, UK

Why bioenergetic organelles contain their own genomes and genetic systems.

Hochberg Georg

Max Planck Institute for Terrestrial Microbiology, Marburg, DE

Rubisco is the central CO₂ fixing enzyme of the Cavin cycle and responsible for the vast majority of all CO₂ fixation on our planet today. In plants, Rubisco undergoes an elaborate set of steps involving the sequential action of at least 6 different dedicated folding and assembly chaperones to assemble into its enzymatically active form. This complexity evolved from much simpler Rubisco ancestors that functioned without any of these additional factors. In this talk I will summarize my lab’s work on retracing the evolution of Rubisco’s complex present-day assembly requirements.

Martin William

Institut für Molekulare Evolution, Heinrich-Heine-Universität Düsseldorf, DE

GTP before ATP: The very early evolution of energy currencies preserved in modern metabolism.

Chloroplasts and mitochondria are the bioenergetic organelles of eukaryotic cells. Their energy conservation entails ion pumping and the ATP synthase. Before the origin of chemiosmosis, there had to be simpler mechanisms of energy conservation and other currencies of biochemical energy. In my talk I will suggest that key pieces of that puzzle, hitherto overlooked, are hiding in plain sight in the metabolism of modern cells.

4. Mechanistic aspects of electron transfer and electron bifurcation

Osyczka Artur

Department of Molecular Biophysics, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, PL

Molecular basis of efficient quinone turnover in photosynthetic and respiratory cytochromes bc.

I plan to discuss recent spectroscopic and structural advances regarding the quinol oxidation /quinone reduction reactions in this group of proteins : in particular focusing on cyt bc1 and cyt b6f. This will be based on presentation of our new (not published yet) exciting data, including the cryo-EM structures and QM calculations that give us new structural and mechanistic insights into the operation of quinone binding sites. I will also discuss some aspects of the regulatory role of these complexes (like involvement of cyt b6f in cyclic electron transfer)

Schuller Jan

SYNMIKRO Research Center and Department of Chemistry Philipps University Marburg, DE

Molecular Basis of Biological CO2 Fixation – Dissecting the Wood-Lijughdal pathway: I will talk about bioenergetic and redox proteins from acetogens and methanoarchaea. In theory, also topic 6 could fit – I will show structural studies of amazing respiratory/bioenergetic complexes.

5. Bioenergetics and biosynthesis involving bioblasts of photosynthetic organisms

Burlacot Adrien

Carnegie institution for Science, Washington D.C., US

How does photosynthetic electron transport responds to light fluctuations?

Photosynthetic organisms use sunlight energy to trigger electron transport reactions in the chloroplast that lead to CO2 fixation and biomass building blocks. However, in natural environment, they are subject to vast and frequent fluctuation in the light intensity to which they have to acclimate to. Here we show that the partitioning of photosynthetic electrons between various electron routes is critical for photosynthetic acclimation to a wide diversity of light fluctuation patterns.

Krieger-Liszkay Anja

Institute for Integrative Cell Biology (I2BC), Paris, FR

A complex and dynamic redox network regulating oxygen reduction at photosystem I.

Thiol-dependent redox regulations play a central role in regulating photosynthesis. Using EPR spin-trapping and a collection of redoxin mutants, we show that superoxide generation at photosystem I is redox controlled.

Roach Thomas

University of Innsbruck, Department of Botany, AT

Photosynthetic flexibility enables balancing primary metabolism for algal growth.

Rutherford Bill

Faculty of Natural Sciences, Department of Life Sciences, Imperial College London, UK

Oxygenic photosynthesis with less energy: breaking the red limit: Chlorophyll-f-containing long-wavelength photosystems break through the energy limitations that seem to constrain the conventional chlorophyll-a-based oxygenic photosynthesis. Our latest spectroscopic and biophysical studies provide new structural and mechanistic understanding of these remarkable photo-oxidoreductases.

Viola Stefania

Institute of Biosciences and Biotechnologies of Aix-Marseille, FR

Redox regulation of chloroplast antioxidant network and ATP-synthase activity by the CDSP32 thioredoxin.

I will talk about the roles of the atypical CDSP32 thioredoxin in chloroplast redox homeostasis through the regulation of both enzymatic antioxidant network and photosynthesis. I will present our recent work showing that CDSP32 is involved in the redox regulation of the chloroplast ATP synthase activity during dark/light and light/dark transitions.

6. Electron transfer system proteins

Gennis Robert

Department of Chemistry, University of Illinois, US

Kaila Ville

Wallenberg Academy Fellow, Department of Biochemistry and Biophysics, Stockholm University, SE

Deciphering the molecular mechanism of proton-electron coupling in the Complex I machinery.

Letts James

University of California, Davis

Diversity of respiratory supercomplexes: The respiratory chain supercomplexes have been structurally and functionally characterized from only a small number of model organisms. An aim in my lab is to examine respiratory complexes from previously uncharacterized species to better understand the variability and conservation of their composition and key structural elements.

Michel Hartmut

Max Planck Institute of Biophysics, DE

Keynote: CryoEM structures of intermediates of the catalytic cycle of cytochrome c oxidase.

Raman CS

University of Maryland School of Pharmacy, Baltimore, US

Innovations in Bacterial Breathing: Hardwired Respirasomes: Thus far, it is widely believed that bacterial respirasomes do not exist. Here, I will present surprising new details regarding how my laboratory discovered the widespread occurrence of previously unknown self-sufficient macromolecular machines, which can not only couple the oxidation of virtually any electron donor to the reduction of dioxygen, but simultaneously achieve energy conservation as well. Notably, I will show convincing physiological, biochemical, and structural results to highlight the extraordinary mechanistic diversity that drives prokaryotic aerobic respiration.

Sazanov Leonid

Institute of Science and Technology, AT

Complex I mechanism – the latest developments.

7. Respiratory complexes and supercomplexes - structure and function

Ädelroth Pia

Department of Biochemistry and Biophysics, Stockholm University, SE

The branched respiratory chain in Mycobacteria.

Djurabekova Amina

Department of Physics, University of Helsinki, FI-00014, Helsinki, FI

ECI: Analysis of the Atomistic MD Simulations of CI+CIII Interactions and Associated Lipid Binding.

Enríquez Jose-Antonio

National Center for Cardiovascular Research Carlos III, Madrid, ES

Respiratory chain heterogeneity for healthy metabolism.

Kühlbrandt Werner

Max Planck Institute of Biophysics, Frankfurt, DE

High-resolution cryoEM of energy-converting complexes in mitochondria: My talk will present our latest results on the structures of mitochondrial membrane protein complexes, in particular ATP synthase, complex I and its supercomplexes, determined by high-resolution cryoEM, including high-resolution cryo-tomography of the complexes in situ.

Larsson Nils-Goran

Division of Molecular Metabolism, Department of Medical Biochemistry and Biophysics (MBB), Karolinska Institutet, Stockholm, Sweden

The organization of the respiratory chain and metabolic disease: I will talk about ongoing genetic studies of the role for respirasomes in the mouse, and also describe metabolic consequences of altered stoichiometry between dehydrogenases feeding electrons into the Q pool.

Marechal Amandine

University College London, UK

I will talk about the complexes and supercomplexes of the yeast electron transfer system.

Pereira Manuela

Faculty of Sciences, University of Lisbon, PT

Respiratory monotopic proteins from S. aureus: Prokaryotes, in comparison to eukaryotes, present much more robust, diversified, and flexible respiratory chains, with proteins capable of using different organic or inorganic compounds as an energy source and a diversity of electron acceptors. This diversity is also achieved by the presence of multiple monotopic quinone reductases that allow the connection between various catabolic pathways and the respiratory chain. Because monotopic proteins interact with only with one leaflet of the lipid bilayer, they do not directly contribute to the electrochemical potential, but nevertheless they are important to the buildup of such potential since they all produce quinol, which is oxidized by redox-driven charge translocation proteins. Despite their importance, monotopic proteins have not been intensively studied. We will present our study on different monotopic proteins involved in the respiratory chain of S. aureus.

Vercellino Irene

Jülich Research Center, DE

SCAF1 drives the compositional diversity of mammalian respirasomes.

The talk will focus on the structural investigation of mammalian respiratory supercomplexes by cryo-EM. Our work enabled the identification and characterization of two sets of supercomplexes, one dependent on the assembly factor SCAF1 and the other independent from it.

Zdorevskyi Oleksii

Department of Physics, University of Helsinki, FI-00014, Helsinki, FI

ECI: Long-range charge transfer in respiratory complex I: an insight from multi-scale molecular dynamics simulations.

8. Redox control of coenzymes and prosthetic groups in electron transfer: NADH, FADH₂, Q, cytochromes

Friedrich Thorsten

University of Freiburg, Institute of Biochemistry, Freiburg im Breisgau, DE

Quinone chemistry in E. coli respiratory complex I.

9. ATPases (F-type, V-type)

Carraro Michela

University of Padova, IT

Disentangling the mitochondrial permeability transition: The mitochondrial permeability transition (PT) is a sudden increase of the permeability to ions and solutes of the inner membrane in response to matrix Ca2+. This process is mediated by a high-conductance and unselective channel, the PT pore (PTP), the molecular identity of which animated an intense debate in the field. Over the last ten years, reconstitution and site-directed mutagenesis studies revealed a central role of the mitochondrial ATP synthase in PTP formation. And yet, a PT can also be mediated by the adenine nucleotide translocator (ANT). Our current work aims at understanding two main aspects: (1) the molecular mechanism that converts the ATP synthase into a channel and (2) the functional cross-talk between ATP synthase and ANT. Our findings show that ANT interacts with specific subunits of the ATP synthase that are major candidates for channel formation, hinting at a possible mutual modulation. Recent high-resolution structures suggest that subunit e (a dimerization subunit of the ATP synthase) contacts the lysolipids filling the rotor through its C-terminus and that Ca2+-dependent conformational changes alter this region. As also proposed by others, this particular contact might modulate c-ring occupancy by lipids via a push-pull mechanism, determining channel formation within the rotor. Our data on HeLa cells deleted for subunit e C-terminus reveal that in mutant cells ANT predominates, indicating that the channel-forming ability of the F-ATP synthase is compromised.

Kane Patricia

SUNY Upstate Medical University, Syracuse, US

Regulation of V-ATPase assembly in aging and disease: Reversible disassembly of V-ATPases is a general mechanism for controlling ATP-driven proton transport across organelle membranes in many cell types. We are exploring the mechanisms regulating reversible disassembly in yeast and mammalian cells. Compromised V-ATPase assembly can lead to shortened lifespan and neurodegenerative or other diseases.

Noji Hiroyuki

University of Tokyo, JP

Engineering of ATP synthase: We attempt to double/triple the gear ratio of the Fo motor in ATP synthase, i.e., H+ per turn, which defines the H+/ATP ratio. For this purpose, we redesigned the peripheral stalk connecting the stator portion of F1 and Fo.Structural and functional analysis of this ATP synthase will be presented.

Stewart Alastair

The Victor Chang Cardiac Research Institute, Darlinghurst, AU

Visualizing inhibition and cooperativity in ATP synthase: Regulation: By imaging E. coli ATP synthase in the presence of ADP or ATP, we have observed movements within the central rotor that suggest how inhibition may be linked to the enzyme’s load. Cooperativity: By imaging mutations in thermophilic F1-ATPase under a range of conditions, we have described key regions of the enzyme involved in the coordinated hydrolysis of ATP.

Sir Walker John

Nobel Prize in Chemistry 1997
MRC Mitochondrial Biology Unit, University of Cambridge, UK

Keynote

Zíková Alena

Laboratory of Functional Biology of Protists, Biology Center CAS, Institute of Parasitology, České Budějovice, CZ

Reversal of ATP synthase as a key feature for the programmed differentiation of insect and mammalian forms of the parasite Trypanosoma brucei: Trypanosoma brucei, a medically important parasite, utilizes both activities of FoF1-ATP synthase during its complex digenetic life cycle. In the insect, the parasite uses the forward activity to generate ATP, while in the mammalian host, it employes the reverse activity to maintain the mitochondrial membrane potential. Using an in vitro differentiation system for the insect forms, we have mapped an intriguing mitochondrial reorganization that enables the reversal of ATP synthase, a key feature that allows the parasite to develop into the infective mammalian form.

10. Transporters and channels - lipids, proteins, ions

Seifert Erin

Thomas Jefferson University, Philadelphia, US

Mitochondrial phosphate carrier depletion in skeletal muscle and Ca2+ homeostasis: the role of mitochondria in cellular Ca2+ homeostasis has long been of interest, and studies have supported a role for mitochondrial Ca2+ in different aspects of cell function, though the underlying mechanisms are not always evident or straightforward to test. Continued investigation on how mitochondria handle Ca2+ may help in this regard. Mitochondrial Ca2+ handling has three components, influx, efflux and chelation. Studies in the molecular era of mitochondrial Ca2+ handling have focused on the first two components, but far less on the chelation. We have attempted to fill this gap using a mouse model in which the mitochondrial inorganic phosphate carrier, PiC, the major Pi transporter in mitochondria, is targeted in the skeletal muscle.

Szewczyk Adam

Nencki Institute of Experimental Biology, Warsaw, PL

Mitochondrial potassium channels: new properties and function.

An overview of our new findings on the properties of mitochondrial large-conductance calcium-activated and ATP-regulated potassium channels will be presented. This will concern the role of mitochondrial potassium channels in cellular senescence, and interactions with other mitochondrial proteins or small molecules such as quercetin, hemin/hydrogen sulfide and infrared light.

11. Small molecule transport across the mitochondrial inner membrane

Indiveri Cesare

University of Calabria, Arcavacata di Rende and CNR IBIOM, Bari, IT

ATP dependence and antiport/uniport switch of the essential amino acid transporter SLC7A5 (LAT1): molecular basis and pathophysiology.

SLC7A5 also known as LAT1 is mainly located at the Blood Brain Barrier and Placenta Barrier and is also strongly over-expressed in all human cancers. We described the antiport cycle of LAT1 by computational analysis, the regulation by cholesterol and ATP, and the ability to switch from antiport to uniport mechanism. Furthermore, we characterized the surprising ability of LAT1 to transport copper in the form of Cu2+-histidinate by a uniport mechanism, with important implications for human health.

Kunji Edmund

MRC Mitochondrial Biology Unit, University of Cambridge, UK

Charge movements during adenine nucleotide exchange by the mitochondrial ADP/ATP carrier.

The mitochondrial ADP/ATP carrier, also called adenine nucleotide translocase, exchanges ADP and ATP across the mitochondrial inner membrane to replenish the eukaryotic cell with metabolic energy. The carrier exists and functions as a monomer, has a single substrate binding site, and operates with a ping-pong kinetic mechanism. This mechanism means that the triply negatively charged ADP molecule first needs to be imported against the membrane potential, before the quadruply negatively charged ATP molecule is exported with the membrane potential. In this talk, we explain how the mitochondrial ADP/ATP carrier accomplishes this remarkable feat to achieve high directional exchange rates in the presence of a large membrane potential.

Palmieri Ferdinando

University of Bari, IT

Keynote: The SLC25 mitochondrial carrier family: identification, properties and physiopathology.

Shen Hongying

Cellular & Molecular Physiology, Yale School of Medicine , Systems Biology Institute, Yale West Campus Orange, Connecticut, US

The Guardians of Mitochondrial Metabolism: Solute Carrier SLC25 Family Transporters: I will likely discuss our work towards the understanding of small molecular metabolite transport through the SLC25 family transporter proteins and their regulation.

Tavoulari Sotira

University of Cambridge, UK

Pathogenic mechanisms by the mitochondrial aspartate/glutamate carrier mutations in citrin deficiency.

My talk will focus on citrin, the mitochondrial aspartate/glutamate carrier isoform 2, which is structurally and mechanistically the most complex SLC25 family member. The absence or dysfunction of citrin leads to citrin deficiency, a highly prevalent pan-ethnic mitochondrial disease. I will present new insights on the role of citrin domains in the transport mechanism and mitochondrial localisation and how these domains contribute to distinct pathogenic mechanisms in citrin deficiency.

12. Uncouplers and proteins with uncoupling function

Axelrod Christopher

Pennington Biomedical Research Center, Baton Rouge, US

Bioenergetic Efficiency in Cell Fate and Survival.

Mitochondria are evolutionarily conserved organelles that mediate cell survival by conferring energetic plasticity and adaptive potential. As such, modifying the fraction of useful energy converted to work has grave implications on cellular fitness. I will discuss emerging evidence linking the fine-tuning of bioenergetic efficiency to the progression of diseases related to uncontrolled cellular expansion such as obesity and cancer.

Bertholet Ambre

University of California Los Angeles, US

I’ll certainly be talking about the use of the patch-clamp technique applied to mitochondria to determine mitochondrial thermogenic capacities. I’ll be talking about H+ current, UCP1 and the ADP/ATP carrier.

Cannon Barbara

Stockholm University, SE

Regulating the activity of mouse and human UCP1: UCP1 is not leaky i.e. its acute activity is a consequence of a balance between stimulatory and inhibitory factors. Here we analyse this interplay, with UCP1 in different tissue environments.

Crichton Paul

Norwich Medical School, Biomedical Research Centre, University of East Anglia, UK

The atomic resolution structure of UCP1

UCP1 is the defining uncoupling protein, facilitating thermogenic energy expenditure in brown adipose tissue. Here, I will discuss recent cryo-EM structural data on UCP1 and new insights on the molecular mechanism of UCP1 activity and regulation.

Fiermonte Giuseppe

University of Bari Aldo Moro, IT

Fraternal Twins with Distinct Metabolic Functions. In my presentation, I will discuss how UCP2 and UCP3, despite sharing approximately 70% sequence identity and transporting the same substrates in vitro, exhibit distinct metabolic functions.

Pohl Elena

University of Veterinary Medicine, Vienna, AT

Uncoupling proteins – proton or fatty acid anion transporter?

The mitochondrial uncoupling proteins (ATP/ADP carrier, UCP1) transport protons across the inner mitochondrial membrane by an unknown mechanism. I will discuss putative mechanisms that describe proteins as either proton carriers that function in the presence of long-chain fatty acids (FA), or FA anion transporters (fatty acid cycling mechanism). A four-steps mechanism for the “sliding” of the FA anion from the matrix to the mitochondrial intermembrane space supporting the latter hypothesis will be presented.

13. Bioenergetic organelle biogenesis, protein assembly and function

Barrientos Antonio

University of Miami Miller School of Medicine, Miami, US

Role of HIGD proteins in controlling respiratory complex assembly and function.

Heberle Joachim

Freie Universität Berlin, Department of Physics, Molecular Biophysics, DE

Infrared Nanoscopy and Tomography of Intracellular Structures.

Ott Martin

Department of Medical Biochemistry and Cell biology, University of Gothenburg, SE

Early steps in the biogenesis of mitochondrial encoded proteins.

Pfanner Nikolaus

Institute of Biochemistry and Molecular Biology, Faculty of Medicine, University of Freiburg, DE

Mitochondrial machineries for import and assembly of proteins: Mitochondria contain more than 1,000 different proteins. The vast majority of proteins are imported from the cytosol. The talk will present the five major pathways of mitochondrial protein import and sorting and discuss the molecular mechanisms and machineries for protein translocation. This will include the translocase of the outer membrane (TOM), the sorting and assembly machinery (SAM), the mitochondrial import (MIM) complex, the mitochondrial intermembrane space import and assembly (MIA) system, the presequence translocase of the inner membrane (TIM23) and the metabolite carrier translocase (TIM22).

Rampelt Heike

Institute of Biochemistry and Molecular Biology, ZBMZ, University of Freiburg, DE

The role of MICOS in respiratory chain assembly.

Ugalde Cristina

Research Center, 12 de Octubre University Hospital, Madrid, ES

Of free CI and the respirasomes: Which came first, the chicken or the egg? I will be talking about how the assembly pathway of CI proceeds until its final fate in the respirasomes.

Zickermann Volker

Institute of Biochemistry II, Goethe University Frankfurt – Medical Faculty, Campus Riedberg, Biocenter, DE

Structural basis of complex I assembly and cardiolipin remodeling in mitochondria.

14. Organelle dynamics

Giordano Francesca

Institute for Integrative Biology of the Cell/CNRS, Paris, FR

Unveiling the Secrets of the Mitochondria-Endoplasmic Reticulum-Lipid Droplet Junction: Functional and Morphological Insights

We have recently shown that Mitochondria-associated Endoplasmic Reticulum [ER] membranes (MAM) are key places for lipid droplet (LD) biogenesis, identifying a novel Mitochondria-ER-LD connection that we have termed MAM-LD contact sites. In my presentation, I will delve into the latest findings from our team elucidating the morphological, molecular, and functional features of this tripartite interaction. Specifically, I will highlight the involvement of the lipid transfer proteins ORP5/ORP8 and of their newly identified binding partners at MAM-LD contact sites.

Khacho Mireille

Mitochondrial Dynamics & Regenerative Medicine, Department of Biochemistry, Microbiology & Immunology, Faculty of Medicine, University of Ottawa, CA

Mitochondrial regulation of muscle stem cells in diseases and aging: I will discuss our discoveries of how mitochondria act as signalling centers that direct the fate of msucle stem cells. We have fund that this is regulated by OPA1 and mitochondrial dynamics. In addition, loss of OPA1 or mitochondrial dynamics, which occurs in aging and neuromuscular diseases, is a major contributing etilogical factor in loss of stem cell function and maintenance.

Shirihai Orian

Department of Molecular and Medical Pharmacology, UCLA, University of California, Los Angeles, US

Keynote

15. Mitochondrial physiology and pathology

Capitanio Nazzareno

University of Foggia, IT

Glancy Brian

NHLBI and NIAMS, National Institutes of Health, Bethesda, US

Loss of TMEM65 causes mitochondrial disease mediated by mitochondrial calcium: I will discuss our recent work identifying Tmem65 as a novel regulator of mitochondrial calcium efflux and how reducing mitochondrial calcium import can rescue the mitochondrial disease associated with Tmem65 loss.

Petersen Ole

Director of Academia Europaea’s Cardiff University Knowledge Hub, UK

Mitochondrial Ca2+ handling in epithelial cells.

Szabó Ildikó

Department of Biology, University of Padova, IT

Redox cycler based therapeutic option against mitochondrial pathologies linked to respiratory chain dysfunction.

Tiranti Valeria

IRCCS Foundation Carlo Besta Neurological Institute, Milan, IT

Recreating Leber’s Hereditary Optic Neuropathy in iPS derived Neurons: Shedding Light on Pathogenic Mechanisms to Combat Blindness: Leber’s hereditary optic neuropathy (LHON), a maternally inherited disease associated with homoplasmic mtDNA mutations, presents challenges in achieving effective therapies. Despite being characterized by selective degeneration of retinal ganglion cells (RGCs) and being the most frequent mitochondrial disease leading to blindness in young individuals, our understanding of its pathogenic mechanisms is hindered by the lack of appropriate models, traditionally investigated in non-neuronal cells. However, emerging effective in-vitro models offer promise in accelerating our understanding of LHON pathophysiology and testing therapeutic strategies for translation into clinical practice, thus benefiting future LHON patients.

Wieckowski Mariusz

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, PL

Metabolic dysfunction in fibroblasts derived from patients with mitochondrial membrane protein-associated neurodegeneration – hope for pharmacological treatment?
Mitochondrial membrane protein-associated neurodegeneration (MPAN), is related to autosomal recessive or dominant mutation in C19orf12 gene encoding mitochondrial membrane protein, however the molecular mechanism underlying MPAN as well as the role of C19orf12 protein in the pathogenesis of the disease is still not fully understood. Investigating mitochondrial and metabolic function using fibroblasts derived from patients with MPAN not only enhances our knowledge about the disease but also helps in development of possible treatment strategies.

Wallace Douglas

Center for Mitochondrial and Epigenomic Medicine at Children’s Hospital of Philadelphia, US

Keynote

16. Mitochondrial reprogramming in health and disease

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17. Functions of apoptotic proteins beyond apoptosis

Gross Atan

Department of Biological Regulation, The Weizmann Institute of Science, IL

Is mitochondrial metabolism involved in apoptosis regulation? Apoptosis is known to involve the release of cytochrome c, however it is not known whether mitochondrial metabolism is involved in this critical decision. Mitochondrial carrier homolog 2 (MTCH2) acts as the mitochondrial receptor for pro-apoptotic tBID, the inducer of cytochrome c release. MTCH2 knockout results in a dramatic change in cellular metabolism and thus we envision that tBID-MTCH2 interaction may also lead to metabolic changes that are prerequisite for cytochrome c release.

Hajnoczky Gyorgy

MitoCare Thomas Jefferson University, Philadelphia, US

Bcl-xL helps to keep mitochondria connected with the endoplasmic reticulum.

Scorrano Luca

University of Padua, Padua, IT

Keeping mitochondria in shape: a matter of life and death.

Walensky Loren

Dana-Farber Cancer Institute, Boston, US

The Janus Faces of MCL-1: Metabolic Regulator by Day and Death Antagonist by Night: MCL-1 is a cardinal regulator of mitochondrial apoptosis, responsible for maintaining cellular life in the face of unexpected cellular stress. Why MCL-1 is cancer’s top choice among BCL-2 family anti-apoptotic proteins for overexpression has been a mechanistic mystery. In investigating additional roles for MCL-1 during homeostasis and disease, we uncovered that MCL-1 dependent cancer cells specifically rely on fatty acid oxidation as a fuel source – a metabolic wiring enforced by MCL-1 itself. Metabolomic, proteomic, and genomic profiling confirmed that the regulation of fatty acid oxidation by MCL-1 is independent of its anti-apoptotic functionality. These data inform novel opportunities to overcome treatment-resistant cancer by targeting the multifaceted roles of MCL-1.

18. Oxygen kinetics – hypoxia to hyperoxia, oxygen sensing, reactive oxygen species

Chinopoulos Christos

Department of Medical Biochemistry, Semmelweis University, HU

Mitochondrial bioenergetics in hypoxia: there is more than OXPHOS.

Hand Steven

Department of Biological Sciences, Louisiana State University, US

Energetic challenges during cellular arrest in an invertebrate extremophile: Features of the F₁F_o ATP synthase.

Sommer Natasha

Department of Pneumology, Medical Clinic II, Excellencecluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Center (DZL), Justus-Liebig-University Giessen, DE

Breath to breath adaptation to hypoxia – acute mitochondrial oxygen sensing in the pulmonary vascular system.

19. Prokaryotic metabolism and microbes as drug targets

Cook Gregory

Queensland University of Technology, Brisbane, AU

Development of dual-targeting inhibitors of mycobacterial energetics to combat multidrug-resistant strains of Mycobacterium tuberculosis.

We report on the discovery of inhibitors targeting multiple components of the mycobacterial respiratory chain. These inhibitors sterilize replicating and non-replicating cultures of Mycobacterium tuberculosis and are synergistic with frontline tuberculosis (TB) drugs pathing the way for novel regimens to treat TB disease.

Fritz-Steuber Julia

University of Hohenheim, Stuttgart, DE

The Na⁺ -translocating NADH:quinone oxidoreductase from pathogenic bacteria: essential redox pump and promising target for antibiotics.

Respiration in many pathogenic bacteria relies on NADH oxidation by a unique, Na⁺ -translocating NADH:quinone oxidoreductase (Na⁺-NQR). Based on 3D structures of Na⁺ -NQR in different states, a mechanism of Na⁺ -NQR is proposed which is based on conformational coupling of electron transfer and Na+ translocation reaction steps. By crystallographic fragment screening, small molecules binding to the active site of Na⁺ -NQR from V. cholerae, Pseudomonas aeruginosa and Klebsiella pneumoniae were identified which are the basis for the development of novel antibiotics

Magalon Axel

Laboratory of Bacterial Chemistry, Marseille, FR

Draw me an oxidoreductase reacting with quinones.

Redox processes are at the heart of energetic metabolism that drives Life on Earth. By extension, complex and efficient electron transfer wires are necessary to connect the different metabolic pathways often located in distinct cellular compartments. Here, we have uncovered a new structural module that, in prokaryotes, enables quinone channeling from the membrane to various water-soluble redox catalytic units.

20. Role of mitochondrial bioenergetics in infection and immune function

Rial Eduardo

Centro de Investigaciones Biológicas Margarita Salas, CSIC, ES

21. From mitochondrial monitoring in organ transplantation to mitochondrial transplantation

Andera Ladislav

Institute of Biotechnology CAS, Vestec, CZ

Pro-apoptotic Bax and Bak proteins modulate mitochondrial respiration via regulation of TEFM expression.

CRISPR-Cas9-mediated elimination of both pro-apoptotic Bax and Bak proteins expression affected mitochondrial respiration in human cancer cells via modulation of mitochondrial factor TEFM protein levels. In Bax/Bak-/- human glioblastoma cells U87 protein but not RNA levels of TEFM were upregulated leading to upregulation of mitochondria-encoded gene expression and boosted respiration as well as in vitro proliferation and cancer growth of U87 cells. Interestingly, the elimination of Bax+Bak expression in human B cell lymphoma HBL-2 cells led to suppression of TEFM protein levels, attenuated respiration, and growth of these cells, pointing to cell-type specific effect of Bax/Bak proteins on mitochondrial gene expression and mitochondrial respiration.

Becker Lance

Northwell Health, Feinstein Institutes for Medical Research, Department of Emergency Medicine, Manhasset, New York, US

Mitochondrial Transplantation Insights: From Concept, to Controversy, to Clinical Trials.

I will present new emerging data from the field of mitochondrial transplantation, which is an attempt to replace dysfunctional mitochondrial via the transplantation of fresh functional exogenous mitochondria into tissues. Examples from our work with mitochondrial transplantation to salvage ischemic tissue will be presented along with the many major questions that exist for this developing science.

Lindeman Jan

Department of Surgery Leiden University Medical Centre, LUMC, Leiden, NL

Ischemia reperfusion injury: driven by reductive rather than oxidative stress? Observations from clinical kidney transplantation.

Meszaros Andras

Medical University of Innsbruck, AT

Impact of steatosis and cold ischemia time on mitochondrial respiration in human liver allografts: to address this issue, we monitor mitochondrial bioenergetics during ex-vivo machine perfusion of liver and kidney to predict graft quality and outcome after organ transplantation.

Schlegel Andrea

Lerner Research Institute, Cleveland Clinic Ohio, Cleveland, US

Current practice of mitochondrial monitoring in organ transplantation: in my presentation I would include the following: current clinical practice of donor and organ viability assessment using mitochondrial injury and function, link the clinical practice to underlying mechanisms explored with experimental transplant models and include different organs (i.e., livers, kidneys, hearts and lungs).

22. Exercise, nutrition, and the bioenergetics of aging

Garcia-Roves Pablo

University of Barcelona and Bellvitge Biomedical Research Institute (IDIBELL), ES

Analyzing the Redox Balance of Coenzyme Q, Mitochondrial Membrane Potential, and Respiratory Functions in Skeletal Muscle Post-Exercise: A Comparative Study of Acute Versus Chronic Physical Activity Impacts.

Molina Anthony

University of California San Diego, School of Medicine, US

23. Mitochondrial pathologies – finding solutions

Batthyany Alexander

Pázmány Péter University, Budapest, HU

Carelli Valerio

Department of Neuromotor Sciences IRCCS, University of Bologna, IT

The optic nerve: the tip of the iceberg of mito-neurodegeneration: The optic nerve as target of mitochondrial dysfunction – DOA and OPA1 state of the art – Future therapeutic strategies

Indrieri Alessia

TIGEM – Telethon Institute of Genetics and Medicine, Pozzuoli Institute for Genetic and Biomedical Research (IRGB), CNR Milan, IT

MicroRNAs Modulation: a novel frontier in the treatment of mitochondrial optic neuropathies.

Lenaers Guy

Université d’Angers, FR

Identification of biomarkers reflecting OPA1-related Dominant Optic Atrophy severity to infer patient cohorts eligible to clinical trials.

My talk will present the results of this multi-OMIC analyses, the correlation between clinical and biological data and the identification of the most relevant biomarkers segregating with the evolution of DOA disease.

Massucci Serena

Mitocon, Rome, IT

The Patients’ Perspective.

Palmieri Luigi

University of Bari “Aldo Moro”, IT

Novel cellular models of SLC25A38-related congenital sideroblastic anemia shed light on mitochondrial physiology and pave the way for therapeutic strategies.

Congenital sideroblastic anemia (CSA) is a heterogeneous group of inherited disorders of erythropoiesis characterized by iron overload in the mitochondria of developing erythroblasts. Mutations in the mitochondrial glycine carrier SLC25A38 cause the most common recessive form of CSA. Unfortunately, our understanding of its pathogenic mechanisms is limited, and pharmacological studies have been hindered by the lack of suitable biological models. To overcome these limitations, we generated two different cell models recapitulating the main features associated with this rare anemia, including reduced heme content and respiratory defect. Beside shedding light on the interrelation between heme biosynthesis and mitochondrial iron homeostasis, our results pave the way to new potential therapeutic strategies.

Tiranti Valeria

IRCCS Foundation Carlo Besta Neurological Institute, Milan, IT

Viscomi Carlo

Department of Biomedical Sciences, University of Padova, IT

Votruba Marcela

Ophthalmology Clinic, University Hospital of Wales, Heath Park, Cardiff, UK

Yu-Wai-Man Patrick

University of Cambridge and Moorfields Eye Hospital, London, UK

OPA1 dominant optic atrophy – from disease mechanisms to novel therapies.

Zanna Claudia

Department of Biomedical and Neuromotor Sciences, University of Bologna, IT

Drug repositioning to treat mitochondrial dysfunctions associated with OPA1 mutations: OPA1 may be proposed as a target for the treatment of a larger spectrum of mitochondrial-related neurodegenerations associated with OPA1 mutations, currently without an established cure. We used a ‘drug repurposing’ approach to identify FDA-approved molecules able to rescue the mitochondrial dysfunctions induced by OPA1 mutations and rapidly deployable in clinical trials.

24. EBEC Science Communication - publishers and publishing, science and teaching, dissemination and social media, sustainable conferences

Azzi Angelo

Editor-in-Chief Molecular Aspects of Medicine

Keynote: A talk about scientific discoveries that were initially met with skepticism, such as Alfred Wegener’s proposal of the theory of continental drift, Semmelweis and handwashing, Barry Marshall and Robin Warren with peptic ulcer, all the way to Quantum Mechanics and Albert Einstein’s famous statement, ’God does not play dice with the universe’, and the continued expansion of the universe.

Bernardi Paolo

Member of the editorial boards of Biochimica et Biophysica Acta Bioenergetics (since 1999), Pharmacological Research, Current Opinion in Physiology, Current Research in Physiology, Life Metabolism, Mitochondrial Communications; served for 18 years in The Journal of Biological Chemistry, for 9 years in Frontiers of Physiology, and for 5 years in Archives of Biochemistry and Biophysics and IUBMB Life, Editor-in-Chief of the Mitochondria Section of Cells

From membrane probes to cytochrome c release: I have two specific and connected issues in mind, i.e. the incorrect use of membrane potential probes in the 1990s, which generated an epidemics of artifacts; and a few high profile mistakes in the debate about the bioenergetics consequences of cytochrome c release. No journal is immune from the problem of ambiguity. Thus, I think that the discussion should be kept as general as possible.

Gnaiger Erich

Editor-in-Chief Bioenergetics Communications, Chair of the Mitochondrial Physiology Society

Addressing the ambiguity crisis: The dissemination of scientific disinformation from peer-reviewed literature infiltrates textbooks, educational platforms, and social media. Is there an erosion of public trust in science? Countering disinformation demands a strategy that raises ‘awareness of the inherent ambiguity crisis, complementing efforts to address the well-acknowledged issues of credibility and reproducibility’ [1], [2].

Ioannidis John

Departments of Medicine, of Epidemiology and Population Health, of Biomedical Data Science, and of Statistics, and Meta-Research Innovation Center at Stanford (METRICS), Stanford University, Stanford, California, US

Keynote: Reproducible and useful research: obstacles and progress.

Nicholls David

Buck Institute for Research on Aging, Novato, US

Why do ‘top’ journals accept papers containing egregious bioenergetic errors?
To professional bioenergeticists, the thermodynamic and kinetic constraints on mitochondrial function are self-evident. It is therefore profoundly concerning that high-profile cell biology papers containing fundamental bioenergetic errors, that appear to have evaded the scrutiny of PI’s, co-authors, reviewers and editors, continue to be accepted by ‘top’ journals. This seriously damages the progress and integrity of science, the careers of junior co-authors and the reputation of the journals, and is a profound misuse of public funds. What can be done?

Petersen Ole

Director of Academia Europaea’s Cardiff University Knowledge Hub, UK

Cleaning up the scientific record: ‘Whether academic decency will prevail in our brave new world, or we succumb to senseless overproduction of irrelevant or erroneous papers, is the main challenge that will define future academic progress.’ [ref 1].

Pirkmajer Sergej

Institute of Pathophysiology, Laboratory for Molecular Neurobiology, Faculty of Medicine, University of Ljubljana, SI