Mitochondrial physiology, redox biology, and genetics
(early bird rates apply for the first 100)
What can you expect from MitoPorto 2023?
In this fourth edition of MitoPorto we highlight mitochondrial physiology, redox biology, and genetics. We also welcome communications from scientists with a multidisciplinary interest in mitochondrial research (e.g. in the context of neuroscience, cancer, metabolism). The program will combine keynote lectures with oral communications selected from the abstracts. Poster sessions will allow participants to discuss their work with fellow scientists and extend collaborative networks. After a productive scientific meeting in Porto, why not extend your stay in this European Top Destination, the World´s Leading City Destination of 2022.
Mike Murphy received his BA in chemistry at Trinity College, Dublin in 1984 and his PhD in Biochemistry at Cambridge University in 1987. After stints in the USA, Zimbabwe, and Ireland he took up a faculty position in the Biochemistry Department at the University of Otago, Dunedin, New Zealand in 1992. In 2001 he moved to the MRC Mitochondrial Biology Unit in Cambridge, UK (then called the MRC Dunn Human Nutrition Unit) where he is a programme leader. Murphy’s research focuses on the roles of reactive oxygen species in mitochondrial function and pathology. In particular he has pioneered the targeting of bioactive and probe molecules to mitochondria in vivo. This general methodology is now widely used. Prominent mitochondria-targeted compounds are antioxidants, such as MitoQ, which protects against oxidative damage in ischaemia-reperfusion injury. Murphy and Rob Smith developed MitoQ as an oral drug which has been used in two Phase II trials so far. This work established mitochondria as a relevant drug target and opened up the field of mitochondrial pharmacology. The Murphy group has gone on to create MitoSNO, a mitochondria-targeted nitric oxide donor which is now being developed as a potential therapy for cardiac ischaemia-reperfusion injury, and MitoG to treat diabetes. Recently his work has extended to determining the mechanism by which mitochondria produce free radicals during ischaemia-reperfusion injury in heart attack and stroke. Murphy is Professor of Mitochondrial Redox Biology at the University of Cambridge, a Wellcome Trust Investigator, an MRC Investigator, an honorary research Professor at the University of Otago, New Zealand, a recipient of the Keilin Medal from the Biochemical Society, an honorary Fellow of the Royal Society of New Zealand and a Fellow of the Academy of Medical Sciences (FMedSci). He has published more than 420 peer reviewed papers, which have garnered more than 63,000 citations and he has an h-index of 129.
Laura Greaves is a Principle Investigator and Senior Lecturer in the Wellcome Centre for Mitochondrial Research at Newcastle University where she leads the Stem Cell and Cancer Metabolism Laboratory. She obtained her PhD at Newcastle University studying the role of mitochondrial DNA mutations in colorectal stem cell ageing in 2005 before completing her post-doctoral studies utilising mitochondrial DNA mutations as lineage tracing marks in stem cell populations. She established her own laboratory in 2016 where her team is now focussed on understanding the role of age-associated mitochondrial dysfunction in intestinal stem cell biology and tumorigenesis. The lab uses a wide range of state-of-the-art experimental approaches, ranging from multi-omic analyses of genetically modified mouse models and organoids to multiplex immunofluorescent analyses of mitochondrial function in large human colorectal cancer cohorts. Outside of work Laura is a keen runner and cyclist who lives with her partner Barry and their five year old son Toby.
Mitochondrial diseases encompass a complex genetic landscape, with 99% protein gene-products encoded by the nuclear genome. Yet the tiny mitochondrial DNA itself encodes genes vital to life and mitochondrial biogenesis and accounts for ¾ of all mitochondrial-disease mutations. These diseases show a surprisingly diverse array of variable physical manifestations, age of onset, and severity in patients – even for mutations within the same gene. This tissue and cell-specific variability in the disease presentation necessitates animal model research to understand these phenomena and lead to translational breakthroughs for mitochondrial disease patients. Despite advances in nuclear genome-engineering, animal mitochondrial-DNA has remained resistant to transgenic manipulation. Our team is among only three labs in the world who have generated these pathogenic mitochondrial-DNA mouse models. Work continues on charactering the pathophysiology of these models, and on pre-clinical experimental therapies for these disorders. We are also interested in mouse models where nuclear gene mutations alter mitochondrial DNA mutagenesis or lead to structural mutations in the mitochondrial chromosome.
Vanessa A. Morais obtained her PhD degree from ITQB/FCT-UNL, Lisbon - Portugal. Her PhD involved a long-term stay as a visiting scholar at the CNDR at UPENN, Philadelphia, USA, in the laboratory of Prof. Dr. Virginia M.-Y. Lee. After her PhD, Vanessa went on with her postdoctoral studies at VIB, Leuven, Belgium, in the laboratory of Prof. Dr. Bart de Strooper; with a long-term stay at VIMM, Padua, Italy, in the laboratory of Prof. Dr. Luca Scorrano. In 2009, Vanessa became a Staff Scientist at VIB and an Associate Professor at KULeuven, Belgium. In 2015, Vanessa returned to Portugal as a Group Leader at iMM – Instituto de Medicina Molecular, Lisbon; and is also an associate professor at Faculty of Medicine University of Lisbon. Vanessa is head of Mitochondrial Biology and Neurodegeneration laboratory and her research is focused on mitochondrial biology and neurodegeneration.
Our overarching goal is to clarify the intimate crosstalk between the host cell – the neuron – and the powerhouse organelle – the mitochondria. Mitochondria at the synapse have a pivotal role in neurotransmitter release, but almost nothing is known about synaptic mitochondria composition or specific functions. Synaptic mitochondria compared to mitochondria in other cells, need to cope with increased calcium load, more oxidative stress, and high energy demands that sustain neurotransmitter release and synaptic plasticity. Our research interests aim at deciphering the intrinsic properties of synaptic mitochondria and to scrutinize their relevance for the healthy brain. For this, we aim to assess the protein fingerprint, the metabolic profile and fuel preference of synaptic mitochondria; the mitochondrial clearance and biogenesis rates at synapse, as well as the contribution of mitochondrial dynamics to neural stem cell fate. Ultimately, we intend to unveil how disruption of these synapse-specific mechanisms contribute to neurodegeneration.
Michael was born in South Africa, moving to the UK in 1960. He studied Physiology and Medicine in Oxford, 1971-75, then moved to St George’s Hospital Medical School to complete his clinical training, graduating 1978. he worked in clinical medicine in junior hospital appointments 1978-1981 including a period working at a rural hospital in the Transkei, South Africa. He moved to the UCL Department of Physiology to embark on PhD studies 1981 -1984 with Tim Biscoe as supervisor and mentor. He has stayed at UCL Physiology (now the Department of Cell and Developmental Biology) ever since, first as a Royal Society University Research Fellow, then as Reader and Professor. His early research was electrophysiological with an interest in neurotransmitter receptor biology, but he became interested first in the influence of cell metabolism on excitability and then increasingly fascinated by mitochondrial biology, in the dialogue between cell signalling pathways and mitochondria, in the roles of mitochondria in disease and ultimately in the question of whether mitochondrial pathways represent viable therapeutic targets in a variety of disease states.