Giant mitochondria do not fuse and exchange their contents with normal mitochondria

Marian Navratil, Alexei Terman, Edgar A. Arriaga

Research output: Contribution to journalArticlepeer-review

81 Scopus citations


Giant mitochondria accumulate within aged or diseased postmitotic cells as a consequence of insufficient autophagy, which is normally responsible for mitochondrial degradation. We report that giant mitochondria accumulating in cultured rat myoblasts due to inhibition of autophagy have low inner membrane potential and do not fuse with each other or with normal mitochondria. In addition to the low inner mitochondrial membrane potential in giant mitochondria, the quantity of the OPA1 mitochondrial fusion protein in these mitochondria was low, but the abundance of mitofusin-2 (Mfn2) remained unchanged. The combination of these factors may explain the lack of mitochondrial fusion in giant mitochondria and imply that the dysfunctional giant mitochondria cannot restore their function by fusing and exchanging their contents with fully functional mitochondria. These findings have important implications for understanding the mechanisms of accumulation of age-related mitochondrial damage in postmitotic cells.

Original languageEnglish (US)
Pages (from-to)164-172
Number of pages9
JournalExperimental Cell Research
Issue number1
StatePublished - Jan 1 2008

Bibliographical note

Funding Information:
This work was supported by the National Institutes of Health (R01-AG20866) and EAA is supported by an NIH Career Award (1K02-AG21453).


  • Giant mitochondria
  • L6 rat myoblasts
  • Mitochondrial fusion proteins
  • Mitochondrial membrane potential
  • Mitofusin-2
  • OPA1


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