Unexpected nonrandom mitochondrial DNA segregation in human cell hybrids

J. W. Shay, S. Ishii

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Cells from patients with various inherited mitochondrial myopathies have been reported to contain more than one type of mitochondrial DNA (heteroplasmy). It has been suggested that the degree of heterplasmy may be important in the clinical manifestations of these diseases; however, little is known about the origin of inheritance of organellar heteroplasmy in mammalian cells. In order to gain an understanding of mechanisms of genetic transmission of mitochondrial DNA, we have made somatic cell hybrids by fusion of cells containing mitochondrial DNA with differences in their restriction endonuclease patterns. This permits the artificial mixing of mitochondria and the study of mitochondrial DNA segregation patterns. In this report evidence will be presented to show that there are differences in the propagational abilities of mitochondrial genomes in many intraspecies human cell hybrids crosses. This was unexpected since it is generally believed that mitochondrial DNA is under relaxed cellular controls and that random transmission of mitochondrial DNA to daughter cells occurs at mitosis. Mitochondrial DNA from tumorigenic HeLa cells, which is initially present in somatic cell hybrids made by fusion of HeLa cells to nontumorigenic cells, is usually lost after several weeks of continuous cell culture. However, when HeLa cells are fused to other tumorigenic cells, random mitochondrial DNA segregation occurs. Thus the tumorigenicity (perhaps state of differentiation) of the parental cells used in these fusions often correlates with the type of mitochondrial DNA retained.

Original languageEnglish (US)
Pages (from-to)279-284
Number of pages6
JournalAnticancer Research
Volume10
Issue number2 A
StatePublished - Jan 1 1990

Keywords

  • cancer
  • hybrids
  • mitochondria

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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