期刊
NUCLEIC ACIDS RESEARCH
卷 37, 期 6, 页码 1817-1828出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkp018
关键词
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资金
- Swedish Research Council [522-2005-7145]
- Angstromke Wiberg Foundation [868332643]
- Loo and Hans Ostermans Foundation [2006Oste0012]
- Marie Curie Early Stage Training Fellowship
- Swedish Foundation for Strategic Research [A3 04:160f]
- U.S. National Institutes on Health/National Institute on Aging [AG027498]
- Ellison Medical Foundation Senior Scholar Award in Aging [AG-SS-1920]
A number of studies showed that the development and the lifespan of Caenorhabditis elegans is dependent on mitochondrial function. In this study, we addressed the role of mitochondrial DNA levels and mtDNA maintenance in development of C. elegans by analyzing deletion mutants for mitochondrial polymerase gamma (polg-1(ok1548)). Surprisingly, even though previous studies in other model organisms showed necessity of polymerase gamma for embryonic development, homozygous polg-1(ok1548) mutants had normal development and reached adulthood without any morphological defects. However, polg-1 deficient animals have a seriously compromised gonadal function as a result of severe mitochondrial depletion, leading to sterility and shortened lifespan. Our results indicate that the gonad is the primary site of mtDNA replication, whilst the mtDNA of adult somatic tissues mainly stems from the developing embryo. Furthermore, we show that the mtDNA copy number shows great plasticity as it can be almost tripled as a response to the environmental stimuli. Finally, we show that the mtDNA copy number is an essential limiting factor for the worm development and therefore, a number of mechanisms set to maintain mtDNA levels exist, ensuring a normal development of C. elegans even in the absence of the mitochondrial replicase.
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