Redox modulation of the activity of DNA topoisomerase I from carrot (Daucus carota) mitochondria.

Abstract

By now, the molecular mechanisms of redox regulation of gene expression at the transcription level have been studied in most detail in prokaryotes [1]. However, many aspects of redox regulation of gene activity in both nuclear and mitochondrial eukaryotic genomes are considerably less understood [2‐5]. Earlier, we demonstrated [6, 7] that redox conditions have a pronounced effect on the intensity of genetic processes in mitochondria. We showed that oxidation caused by addition of potassium ferricyanide or oxidized glutathione to mitochondria led to activation of transcription and translation. Conversely, reduction caused by addition of sodium dithionite or reduced glutathione to mitochondria significantly suppressed these processes. However, the exact molecular mechanism of redox regulation of mitochondrial gene expression in vivo remains obscure. Earlier, we suggested that the mechanism of redox control of genetic functions in mitochondria consisted of two components, being based on the interaction of a specific redox sensor(s) and regulator(s) of redox response [6]. According to this hypothesis, the glutathione-mediated redox system can function as a redox sensor responding to changes in the redox state of the respiratory chain and redox potential of mitochondria as a whole. However, the transcription regulation factors involved in the response of mitochondria to the changes in redox conditions remain to be identified.