Decreased mitochondrial RNA levels without accumulation of mitochondrial DNA deletions in aging Drosophila melanogaster

Steven R. Schwarze, Richard Weindruch, Judd M. Aiken

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


Declines in electron transport system (ETS) activity have been reported to occur with advancing age in Drosophila melanogaster and many other animals. It has been proposed that these changes are importantly involved in the aging process. ETS decline has been attributed to mitochondrial nucleic acid damage. We analyzed various ages of D. melanogaster (embryos to 60-day- old adults) for the presence of mutated mitochondrial DNA (mtDNA) genomes. Although mtDNA genomes with large DNA deletions (up to 5 kb) were identified, abundance was low and remained constant throughout adult life. Therefore, these mtDNA deletions do not appear to be sufficiently abundant to cause large declines in ETS activity. Next, we analyzed various ages of D. melanogaster for the abundance of four mitochondrial-encoded and two nuclear- encoded ETS transcripts. The abundance of the mitochondrial transcripts declined 5-10-fold, while the nuclear-encoded transcripts declined 2-5-fold with advancing age. Separation of flies on the basis of flight loss was used to distinguish physiologic age from chronological age. Insects capable of flight at 30 days of age were found to have a 4-fold higher abundance of cox I mitochondrial-encoded RNA compared to flightless insects. No difference, however, was apparent in the nuclear-encoded β-ATPase RNA level, suggesting only mitochondrial RNA (mtRNA) declines are associated with life expectancy.

Original languageEnglish
Pages (from-to)99-107
Number of pages9
JournalMutation Research - Mutation Research Genomics
Issue number3-4
StatePublished - May 1998

Bibliographical note

Funding Information:
We thank Dr. Immu Scheffler (University of California-San Diego) for providing the Ip clone, members of our laboratory for helpful discussion throughout the course of this work and Drs. Allen Laughon, Mike Strand and Debbie McKenzie for the helpful criticism of the manuscript. This work was supported by RO1 AG11604, PO1 AG11915 and NIH Training Grant T32 AG00213. This is publication 97-14 from the Madison/VA-GRECC.


  • DNA deletion
  • Drosophila aging
  • Electron transport system
  • Mitochondrial DNA
  • Mitochondrial RNA
  • Polymerase chain reaction

ASJC Scopus subject areas

  • Toxicology
  • Genetics


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