Programmed cell death during microgenesis in a Honglian CMS line of rice is correlated with oxidative stress in mitochondria.

The key role of mitochondria in the integration of apoptosis and oxidative stress in mammals has been documented. In plants, mitochondria are implicated in cytoplasmic male sterility (CMS), programmed cell death (PCD), and oxidative stress. However, to date there has been no evidence presented of the interplay among CMS, PCD and oxidative stress. In this study, we demonstrate that the pollen abortion of Honglian CMS line of rice (Oryza sativa L.) displays a PCD phenotype. A premature loss of microspores was accompanied by several biochemical markers of apoptosis. Analysis of mitochondria revealed that during the PCD process there was disruption of the inner mitochondrial membrane potential in microspores. This disruption was correlated with excess production of reactive oxygen species and down-regulation of the activity of superoxide dismutase (SOD), ascorbate peroxidase (APX) and catalase in mitochondria. The excess accumulation of ROS spanned three stages from pollen mother cell to early-uninucleate stage, and was followed by the occurrence of PCD at meiosis. Our data suggest that the microspores suffered from severe oxidative stress during pollen development. It is likely the chronic oxidative stress triggered the tissue-specific PCD and consequently resulted in the abortion of microspores.