A genome approach to mitochondrial-nuclear communicationin Arabidopsis

Mitochondria depend on the nuclear genome to encode the vast majority of their proteins; in turn they control the expression of certain nuclear genes to maintain proper functioning. In this work, Arabidopsis leaves were employed as a model to study nuclear gene expression in response to inhibition of the mitochondrial electron transport by antimycin A. Microarrays containing 11 514 Arabidopsis expressed sequence tags supplied through the Arabidopsis Functional Genomics Consortium (AFGC) were used. Transcript levels of 579 nuclear genes were increased ≥ 2-fold, and the levels of 584 nuclear genes were decreased ≥ 2-fold after antimycin A treatment. While functions of a large number of the gene products are unknown, others are involved in diverse metabolic activities such as phosphorylation, transcription, and energy metabolism. Data from microarray experiments were repeatable and were confirmed by northern hybridization for specific test genes. It was found through cluster analysis that plant cells show significant common response to chemical inhibition of mitochondrial function, aluminum stress, cadmium stress, hydrogen peroxide and virus infection. The results imply that these stresses may act on mitochondria and the responses are in part mediated by mitochondrial-nuclear communication. Most nuclear-encoded respiratory genes involved in the TCA cycle, electron transport and ATP synthesis did not respond to signals from the inhibited mitochondria, while genes for cytochrome c and alternative oxidase were induced. The result indicates that these two genes may be targets in the transcriptional regulation of the two respiratory pathways.