Project description
Mechanisms of mitochondrial functions activation after fertilisation
The EU-funded MitoZebra project is going to investigate the mechanisms underlying the increase in mitochondrial energy production during embryogenesis. Researchers will employ zebrafish embryos as a model system for vertebrate development to measure mitochondrial translational activity using de novo translation assays and assess its contribution to the assembly of new respiratory chain complexes. The project will explore the fundamental mechanism of the co-regulation of cytoplasmic and mitochondrial translation and will provide insights into activation mechanisms of mitochondrial functions after fertilisation. The early embryo nucleus is transcriptionally inactive, and the project has the potential to discover novel, transcription-independent feedback mechanisms that balance mitochondrial and cytoplasmic translations.
Objective
Mitochondria are well known as the powerhouse of cells and play a vital role in embryo development regulating energy
homeostasis. Mitochondrial function has been studied for decades, although several aspects of mitochondrial metabolism during
development still remain unclear. Which mechanisms are responsible for the continuous increase in respiratory chain activity during
embryogenesis? How does translational activity in the early embryo contribute to this process, and how is the translational activity in
mitochondria coordinated with the translational activity in the cytoplasm?
In my project, I will investigate mechanisms that underlie the increase in mitochondrial energy production during embryogenesis.
Using zebrafish embryos as a model system for vertebrate development, I propose to measure mitochondrial translational activity
with de novo translation assays and assess its contribution to the assembly of new respiratory chain complexes. Also, I will explore
the largely enigmatic mechanism of the co-regulation of cytoplasmic and mitochondrial translation.
My research will provide novel insights into the universal yet poorly understood mechanisms that activate mitochondrial function
after fertilization. Since in the early embryo nucleus is transcriptionally inactive, my work has the potential to discover novel,
transcription-independent feedback-mechanisms that balance mitochondrial and cytoplasmic translations.
Fields of science
Keywords
Programme(s)
Funding Scheme
MSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)Coordinator
1030 Wien
Austria