UK: Conference: MitOX 2023 - 21st April 2023

ABOUT MITOX

The Nuffield Department of Women's & Reproductive Health invites you to MitOX 2023 on Friday 21st April 2023. It's our annual meeting packed with short talks and posters on cancer metabolism, neuroscience, diabetes, mitochondrial disorders and general mitochondrial biology. This one day hybrid conference is ideal for researchers with an interest in mitochondria from both academia and pharma.

https://www.wrh.ox.ac.uk/news/mitox-2023-21st-april


SPEAKERS (at time of posting)

Alex Clarke, The Kennedy Institute, University of Oxford

Dynamic mitochondrial transcription and translation in B cells control germinal centre entry and lymphomagenesis


Mauro Corrado, University of Cologne

Metabolic control of T cell immunity


Afshin Beheshti, KBR at NASA Ames Research Center

Mitochondrial Dysregulation is the Universal Driver Impacting Health During Spaceflight and microRNAs can be Utilized to Mitigate this Response


Laura Greaves, University of Newcastle

Investigating the role of mitochondrial DNA mutations in colorectal cancer progression’


Jaya Palagedara, University of Oxford

Metabolic symbiosis between oxygenated and hypoxic tumour cells: insights from an agent-based mathematical model


Sara Cogliati, CMB-UAM (Madrid)

The plasticity of the electron transport chain shapes metabolism: a sex-biased perspective.


Brian Caffrey, The Rosalind Franklin Institute

Imaging mitochondrial networks across tissues using electron microscopy/spectroscopy


Wayne Frasch, Arizona State University

F1FO ATP synthase molecular motor mechanisms


Dagan Wells /Katharina Spath, University of Oxford

mtDNA Heteroplasmy in oocyte spindle transfer


Aurora Gomez-Duran, CIB-CSIC, Spain

mtDNA variation in health and disease


Ruxandra Dafinca, University of Oxford

Mitochondrial defects in cell models of motor neuron disease

 

Programme announced


9.25 Karl Morten (Oxford) Welcome


General Mitochondria. Chairs: Barbara Kronsteiner-Dobramysl (Oxford) & Sevasti Zervou (Oxford)

9.30 Sara Cogliati (CMB-UAM (Madrid)): The plasticity of the electron transport chain shapes metabolism: a sex-biased perspective

9.55 Brian Caffrey (Rosalind Franklin Institute): Imaging mitochondrial networks across tissues using electron microscopy/spectroscopy

10.20 Robert Glastad (University of Bergen): Mitochondrial network structure modulates cell-to cell mtDNA variability generated by cell divisions

10.35 Katie O’Brien (Cambridge) Putatively adaptive Andean single nucleotide variant in EPAS1 preserves mitochondrial oxygen consumption.

10.50 Coffee


Mitochondrial Medicine. Chairs: Kate Sargent (Oxford) & Jan Willem Taanman (UCL) 11.20 Aurora Gomez-Duran (CIB-CSIC (Madrid)) mtDNA variation in health and disease 11.45 Katharina Spath (Oxford) Heteroplasmy in oocyte spindle transfer

12.10 Ruxandra Dafinca (Oxford) Mitochondrial defects in cell models of motor neuron disease

12.35 Javier Bautista (UCL) Mitochondrial dysfunction is involved in progranulin-associated frontotemporal dementia

12.50 Lunch & Poster session


Immuno-metabolism. Chairs Ana Victoria Lechuga-Vieco (Oxford) & Ilse Pienaar (Birmingham)

14.20 Alex Clarke (Oxford) Dynamic mitochondrial transcription and translation in B cells control germinal centre entry and lymphomagenesis

14.45 Mauro Corrado (University of Cologne) Metabolic control of T-Cell immunity

15.10 Mariana Borsa (Oxford) The role of mitochondrial inheritance in the early rise of asymmetric T cell fates

15.25 Katja Gassner (Bellvitge Biomedical Research Institute, Barcelona) Unravelling the immune response in mitochondrial disease patients


The Pollard Lecture

15.40 Wayne Frasch (Arizona State University) Diversity and Evolution of the F, A, and V-type Family of Rotary Molecular Motors.

16.05 Tea


Cancer. Chairs Rhiannon McGeeham (Portsmouth) & James Chettle (Oxford)

16.35 Laura Greaves (Newcastle) Investigating the role of mitochondrial DNA mutations in colorectal cancer progression’

17.00 Jayathilake Pahala Gedara (Oxford) Metabolic symbiosis between oxygenated and hypoxic tumour cells: insights from an agent-based mathematical model

17.15 Megan Stoker (Oxford) Targeting mitochondrial metabolism as a promising therapeutic strategy in cancer.

17.30 Afshin Beheshti (Broad Institute of MIT & Harvard) MicroRNA Based Mitochondrial Dysregulation as Unifying Driver for Post-Acute Sequelae of COVID-19 (PASC) and Cancer

 

Poster presentations of possible interest

Mitochondrial Dysfunction with Aberrant Expression of Endogenous Retroviral Sequences in Myalgic Encephalomyelitis (ME/CFS)

Karen Giménez-Orenga1, Elisa Oltra2,3

1 Escuela de Doctorado, Universidad Católica de Valencia San Vicente Mártir, Valencia, Spain

2 Department of Pathology, School of Health Sciences, Universidad Católica de Valencia San Vicente Mártir, Valencia, Spain

3 Centro de Investigación Traslacional San Alberto Magno, Universidad Católica de Valencia San Vicente Mártir, Valencia, Spain

Although the underlying pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is still unknown, several hypotheses have been put forward. These include dysregulation and hyperactivation of the immune system, metabolic alterations, and mitochondrial dysfunction. The latter has attracted the most attention, as it could explain many of the symptoms present in ME/CFS. Moreover, an increasing amount of evidence links chronic and complex diseases to mitochondrial disruption.

In this work, we review the mitochondrial research on ME/CFS to date and relate it to an emerging research area focused on the study of human endogenous retroviruses (HERV). HERVs are a superfamily of transposable elements consisting of genomic sequences acquired from ancient exogenous viral infections with potential to produce immune and metabolic disturbances. The reported aberrant expression of these sequences in ME/CFS, in combination with emerging evidence suggesting a relationship between transposable elements and mitochondrial dysfunction, paves the way towards a new research line focused on understanding HERVs involvement in ME/CFS disease.


Myelin: a powerhouse of the brain?

Alessandro Maria Morelli – Genoa (Italy) University.

The human brain contains ~ 500 cm3 of white matter (WM) and ~70 cm3 of gray matter (GM) and the Human is the species with the highest WM/GM ratio among animals 1. WM is made up of more than 50% myelin, so the myelin makes up almost half of the human brain and therefore it is worthwhile to investigate the functions of myelin which have hitherto appeared elusive.

In myelin, the presence of the typically mitochondrial molecular machinery of Oxidative Phosphorylation has been highlighted, which reaches myelin thanks to a dramatic increase in the production of mitochondria in the oligodendrocyte where mitochondria apparently migrate towards myelin along the oligodendrocyte processes. Furthermore, a consistent protein synthesis has been highlighted in the oligodendrocyte processes instructed by typically mitochondrial mRNA which is directed into the processes thanks to a specific 3' UTR motif 2. Interestingly, myelin contains a transcriptome that is more than double that of other brain districts 3 and the proteomic analysis highlighted a high content of typically mitochondrial proteins 4. All these devices dedicated to ATP synthesis give isolated myelin the ability to produce ATP in typically mitochondrial ways at levels higher than those of isolated mitochondria, as has been experimentally verified 5.

Proteolipid (PLP) is the most abundant protein in myelin (45%) whose function appears to be to conduct proton currents 6 and is inserted into the myelin membranes with particular modalities aimed at developing this function. Myelin Basic Protein (MBP) is the second most abundant protein of myelin (28%) and is inserted into membranes in order to develop a putative proton capacitor function, which would accumulate protons due to its basic nature during sleep to make them available during wakefulness in support of ATP synthesis which sustains nerve impulses. The property of accumulating energy in the form of protons is in line with experimentally measurements of the amount of ATP synthesized by isolated myelin pre-incubated with NADH and subsequent removal of NADH: the ATP synthesized is proportionally to the pre-incubation time with NADH 5.

All these findings lead to attributing to myelin a priority role in the processing of energy in the brain which is the organ that alone consumes a fifth of the energy consumed by the human body despite being only about the fiftieth part of the human body. New perspectives open up in the possible understanding of memory and sleep, which are evident energy-dependent processes.