Summary
Mitochondria are essential organelles found in every eukaryotic cell, required to convert food into usable energy. The
mitochondrial oxidative phosphorylation (OXPHOS) system, which produces the majority of cellular energy in the form of
ATP, is controlled by two distinct genomes: the nuclear and the mitochondrial genome (mtDNA). Mutations in mitochondrial
genes encoded by either genome could cause diseases affecting OXPHOS system, called mitochondrial diseases, whose
prevalence has been estimated to be ≈1:8500. Moreover, dysfunction of mitochondrial OXPHOS system has emerged as a
key factor in a myriad of “common” diseases, including neurodegenerative and metabolic disorders like Parkinson’s and
Alzheimer’s Disease, Type 2 Diabetes, and was linked to aging process. Despite all this, it is surprising that our
understanding of the mechanisms governing the mitochondrial gene expression and its associated pathologies remain
superficial and therapeutic interventions unexplored. The basic machineries for mtDNA replication, mtDNA transcription and
mitochondrial translation are known, but the regulation of these processes in response to metabolic demands is poorly
understood. The complex nature of mitochondrial gene expression that relies on two different genomes calls for a
multidisciplinary approach where different teams of researchers join forces. Studies in this area are not only of basic
scientific interest but may also provide new avenues towards treatment of mitochondrial dysfunction in a variety of human
diseases.
The key aim of the REMIX Network is combine the skills of European research groups to provide strategic training of the
next generation of scientists through a programme that will progress in the elucidation of the molecular mechanisms and
pathways that regulate mitochondrial gene expression.
mitochondrial oxidative phosphorylation (OXPHOS) system, which produces the majority of cellular energy in the form of
ATP, is controlled by two distinct genomes: the nuclear and the mitochondrial genome (mtDNA). Mutations in mitochondrial
genes encoded by either genome could cause diseases affecting OXPHOS system, called mitochondrial diseases, whose
prevalence has been estimated to be ≈1:8500. Moreover, dysfunction of mitochondrial OXPHOS system has emerged as a
key factor in a myriad of “common” diseases, including neurodegenerative and metabolic disorders like Parkinson’s and
Alzheimer’s Disease, Type 2 Diabetes, and was linked to aging process. Despite all this, it is surprising that our
understanding of the mechanisms governing the mitochondrial gene expression and its associated pathologies remain
superficial and therapeutic interventions unexplored. The basic machineries for mtDNA replication, mtDNA transcription and
mitochondrial translation are known, but the regulation of these processes in response to metabolic demands is poorly
understood. The complex nature of mitochondrial gene expression that relies on two different genomes calls for a
multidisciplinary approach where different teams of researchers join forces. Studies in this area are not only of basic
scientific interest but may also provide new avenues towards treatment of mitochondrial dysfunction in a variety of human
diseases.
The key aim of the REMIX Network is combine the skills of European research groups to provide strategic training of the
next generation of scientists through a programme that will progress in the elucidation of the molecular mechanisms and
pathways that regulate mitochondrial gene expression.
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More information & hyperlinks
| Web resources: | https://cordis.europa.eu/project/id/721757 |
| Start date: | 01-10-2016 |
| End date: | 31-01-2021 |
| Total budget - Public funding: | 3 920 630,04 Euro - 3 920 630,00 Euro |
Cordis data
Original description
Mitochondria are essential organelles found in every eukaryotic cell, required to convert food into usable energy. Themitochondrial oxidative phosphorylation (OXPHOS) system, which produces the majority of cellular energy in the form of
ATP, is controlled by two distinct genomes: the nuclear and the mitochondrial genome (mtDNA). Mutations in mitochondrial
genes encoded by either genome could cause diseases affecting OXPHOS system, called mitochondrial diseases, whose
prevalence has been estimated to be ≈1:8500. Moreover, dysfunction of mitochondrial OXPHOS system has emerged as a
key factor in a myriad of “common” diseases, including neurodegenerative and metabolic disorders like Parkinson’s and
Alzheimer’s Disease, Type 2 Diabetes, and was linked to aging process. Despite all this, it is surprising that our
understanding of the mechanisms governing the mitochondrial gene expression and its associated pathologies remain
superficial and therapeutic interventions unexplored. The basic machineries for mtDNA replication, mtDNA transcription and
mitochondrial translation are known, but the regulation of these processes in response to metabolic demands is poorly
understood. The complex nature of mitochondrial gene expression that relies on two different genomes calls for a
multidisciplinary approach where different teams of researchers join forces. Studies in this area are not only of basic
scientific interest but may also provide new avenues towards treatment of mitochondrial dysfunction in a variety of human
diseases.
The key aim of the REMIX Network is combine the skills of European research groups to provide strategic training of the
next generation of scientists through a programme that will progress in the elucidation of the molecular mechanisms and
pathways that regulate mitochondrial gene expression.
Status
CLOSEDCall topic
MSCA-ITN-2016Update Date
28-04-2024
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Organisations
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| UNIVERSITAET ZU KOELN (UCO) (Coördinator)
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| GOETEBORGS UNIVERSITET
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| KHONDRION BV
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| MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
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| STICHTING KATHOLIEKE UNIVERSITEIT (SKU/RU)
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| STOCKHOLMS UNIVERSITET
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| THE UNIVERSITY OF CAMBRIDGE
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| UNITED KINGDOM RESEARCH AND INNOVATION
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| UNIVERSITE DE GENEVE
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| UNIVERSITY OF NEWCASTLE UPON TYNE