Summary
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.
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.
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More information & hyperlinks
Web resources: | https://cordis.europa.eu/project/id/895790 |
Start date: | 01-09-2021 |
End date: | 31-08-2023 |
Total budget - Public funding: | 186 167,04 Euro - 186 167,00 Euro |
Cordis data
Original description
Mitochondria are well known as the powerhouse of cells and play a vital role in embryo development regulating energyhomeostasis. 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.
Status
CLOSEDCall topic
MSCA-IF-2019Update Date
28-04-2024
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