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Mitochondrial respiratory chain deficiency in Caenorhabditis elegans results in developmental arrest and increased life span
- Source :
- The Journal of biological chemistry. 276(34)
- Publication Year :
- 2001
-
Abstract
- The growth and development of Caenorhabditis elegans are energy-dependent and rely on the mitochondrial respiratory chain (MRC) as the major source of ATP. The MRC is composed of approximately 70 nuclear and 12 mitochondrial gene products. Complexes I and V are multisubunit proteins of the MRC. The nuo-1 gene encodes the NADH- and FMN-binding subunit of complex I, the NADH-ubiquinone oxidoreductase. The atp-2 gene encodes the active-site subunit of complex V, the ATP synthase. The nuo-1(ua1) and atp-2(ua2) mutations are both lethal. They result in developmental arrest at the third larval stage (L3), arrest of gonad development at the second larval stage (L2), and impaired mobility, pharyngeal pumping, and defecation. Surprisingly, the nuo-1 and atp-2 mutations significantly lengthen the life spans of the arrested animals. When MRC biogenesis is blocked by chloramphenicol or doxycycline (inhibitors of mitochondrial translation), a quantitative and homogeneous developmental arrest as L3 larvae also results. The common phenotype induced by the mutations and drugs suggests that the L3-to-L4 transition may involve an energy-sensing developmental checkpoint. Since approximately 200 gene products are needed for MRC assembly and mtDNA replication, transcription, and translation, we predict that L3 arrest will be characteristic of mutations in these genes.
- Subjects :
- Mitochondrial DNA
biology
ATP synthase
Base Sequence
Mitochondrial translation
Pharyngeal pumping
Protein subunit
Cell Biology
biology.organism_classification
Biochemistry
Molecular biology
Electron Transport
Mitochondrial respiratory chain
biology.protein
Animals
Caenorhabditis elegans
Molecular Biology
Gene
Genes, Helminth
DNA Primers
Subjects
Details
- ISSN :
- 00219258
- Volume :
- 276
- Issue :
- 34
- Database :
- OpenAIRE
- Journal :
- The Journal of biological chemistry
- Accession number :
- edsair.doi.dedup.....cedb634d78650feeb9ec253a91cd45ea