دورية أكاديمية
The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals.
العنوان: | The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals. |
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المؤلفون: | Takayuki Kanazawa, Mauro D Zappaterra, Ayako Hasegawa, Ashley P Wright, Erin D Newman-Smith, Karolyn F Buttle, Kent McDonald, Carmen A Mannella, Alexander M van der Bliek |
المصدر: | PLoS Genetics, Vol 4, Iss 2, p e1000022 (2008) |
بيانات النشر: | Public Library of Science (PLoS), 2008. |
سنة النشر: | 2008 |
المجموعة: | LCC:Genetics |
مصطلحات موضوعية: | Genetics, QH426-470 |
الوصف: | The C. elegans eat-3 gene encodes a mitochondrial dynamin family member homologous to Opa1 in humans and Mgm1 in yeast. We find that mutations in the C. elegans eat-3 locus cause mitochondria to fragment in agreement with the mutant phenotypes observed in yeast and mammalian cells. Electron microscopy shows that the matrices of fragmented mitochondria in eat-3 mutants are divided by inner membrane septae, suggestive of a specific defect in fusion of the mitochondrial inner membrane. In addition, we find that C. elegans eat-3 mutant animals are smaller, grow slower, and have smaller broodsizes than C. elegans mutants with defects in other mitochondrial fission and fusion proteins. Although mammalian Opa1 is antiapoptotic, mutations in the canonical C. elegans cell death genes ced-3 and ced-4 do not suppress the slow growth and small broodsize phenotypes of eat-3 mutants. Instead, the phenotypes of eat-3 mutants are consistent with defects in oxidative phosphorylation. Moreover, eat-3 mutants are hypersensitive to paraquat, which promotes damage by free radicals, and they are sensitive to loss of the mitochondrial superoxide dismutase sod-2. We conclude that free radicals contribute to the pathology of C. elegans eat-3 mutants. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1553-7390 1553-7404 |
Relation: | http://europepmc.org/articles/PMC2265488?pdf=render; https://doaj.org/toc/1553-7390; https://doaj.org/toc/1553-7404 |
DOI: | 10.1371/journal.pgen.1000022 |
URL الوصول: | https://doaj.org/article/a009548353de4a6f95308464f4a45af9 |
رقم الأكسشن: | edsdoj.009548353de4a6f95308464f4a45af9 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 15537390 15537404 |
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DOI: | 10.1371/journal.pgen.1000022 |