Mitochondrial DNA is not fragmented during apoptosis

Marta Murgiai, Paola Pizzo, Dorianna Sandona, Paola Zanovello, Rosario Rizzuto, Francesco Di Virgilio

Research output: Contribution to journalArticle

Abstract

We have exposed mouse thymocytes and P-815 mastocytoma cells to four different conditions reported to cause apoptosis: 1) incubation in the absence of mitogenic factors; 2) incubation in the presence of dexamethasone; 3) stimulation with external ATP; 4) treatment with high concentrations of the K+ ionophore valinomycin. These treatments caused DNA fragmentation to a varying extent in the two cell types. High stringency hybridization with a cDNA probe specific to a mitochondrial DNA sequence revealed that during apoptosis induced by lack of mitogenic factors, dexamethasone, or extracellular ATP, mitochondrial DNA was not fragmented. On the contrary, valinomycin caused extensive degradation of mitochondrial DNA. These results support the notion that DNA fragmentation during apoptosis is a specific nuclear event and suggest that other agents, such as valinomycin, may act less selectively.

Original languageEnglish
Pages (from-to)10939-10941
Number of pages3
JournalJournal of Biological Chemistry
Volume267
Issue number16
Publication statusPublished - Jun 5 1992

ASJC Scopus subject areas

  • Biochemistry

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    Murgiai, M., Pizzo, P., Sandona, D., Zanovello, P., Rizzuto, R., & Di Virgilio, F. (1992). Mitochondrial DNA is not fragmented during apoptosis. Journal of Biological Chemistry, 267(16), 10939-10941.