Abstract

BackgroundCytoplasmic male sterility (CMS) has often been associated with abnormal mitochondrial open reading frames. The mitochondrial gene orfH79 is a candidate gene for causing the CMS trait in CMS-Honglian (CMS-HL) rice. However, whether the orfH79 expression can actually induce CMS in rice remains unclear.ResultsWestern blot analysis revealed that the ORFH79 protein is mainly present in mitochondria of CMS-HL rice and is absent in the fertile line. To investigate the function of ORFH79 protein in mitochondria, this gene was fused to a mitochondrial transit peptide sequence and used to transform wild type rice, where its expression induced the gametophytic male sterile phenotype. In addition, excessive accumulation of reactive oxygen species (ROS) in the microspore, a reduced ATP/ADP ratio, decreased mitochondrial membrane potential and a lower respiration rate in the transgenic plants were found to be similar to those in CMS-HL rice. Moreover, retarded growth of primary and lateral roots accompanied by abnormal accumulation of ROS in the root tip was observed in both transgenic rice and CMS-HL rice (YTA).ConclusionThese results suggest that the expression of orfH79 in mitochondria impairs mitochondrial function, which affects the development of both male gametophytes and the roots of CMS-HL rice.

Highlights

  • Cytoplasmic male sterility (CMS) has often been associated with abnormal mitochondrial open reading frames

  • We investigated the localization of the OrfH79 gene product and found that the protein is mainly present in the mitochondria of CMS-HL rice

  • Similar phenotypes were observed in the YtA line. These results indicate that orfH79 impairs mitochondrial function, which appears to disturb the development of both male gametophytes and the roots of CMS-HL rice

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Summary

Introduction

Cytoplasmic male sterility (CMS) has often been associated with abnormal mitochondrial open reading frames. Inherited cytoplasmic male sterility (CMS) has been described in over 150 plant species [1,2]. The failure of pollen development in a CMS background is suggested to be associated with chimeric open reading frames (ORFs) that have arisen from unusual recombination events in mitochondria [3]. The mitochondrial genome carries important genetic information for a number of eukaryotic functions, including energy metabolism, development, programmed cell death and responses to oxidative stress [6]. The mitochondrial metabolism is usually disturbed by high levels of reactive oxygen species (ROS), generated in response to a range of biotic and abiotic stressors [7,8,9]. The initial trigger of the oxidative stress response remains to be determined

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