A viable hypomorphic mutation in the mitochondrial ribosome subunit, MRPS-31, exhibits mitochondrial dysfunction in C. elegans .
| Autor: | Jozwik KM; Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee, United States., Held JP; Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee, United States., Hecht CA; Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee, United States., Patel MR; Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee, United States.; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee, United States.; Evolutionary Studies, Vanderbilt University, Nashville, Tennessee, United States.; Diabetes Research and Training Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States. |
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| Jazyk: | angličtina |
| Zdroj: | MicroPublication biology [MicroPubl Biol] 2024 Sep 30; Vol. 2024. Date of Electronic Publication: 2024 Sep 30 (Print Publication: 2024). |
| DOI: | 10.17912/micropub.biology.001344 |
| Abstrakt: | The mitochondrial ribosome (mitoribosome) translates mitochondrial genome encoded proteins essential for cellular energy production. Given this critical role, defects in the mitoribosome can cause mitochondrial stress and manifest as multisystemic diseases. In a screen for unique activators of the mitochondrial unfolded protein response (UPR mt ) in Caenorhabditis elegans , we recovered a strain harboring a missense mutation in the gene encoding mitochondrial ribosome protein S31 ( MRPS-31 )-a component of the mitoribosome small subunit. Herein, we confirm causality of the mrps-31 allele and characterize its induction of UPR mt and impact on organismal development, providing a valuable model for further study of the mitoribosome. Competing Interests: The authors declare that there are no conflicts of interest present. (Copyright: © 2024 by the authors.) |
| Databáze: | MEDLINE |
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