Effect of mitochondrial dysfunction on carbon metabolism and gene expression in flower tissues of Arabidopsis thaliana

MARIA V. BUSI*; MARIA E. GOMEZ-LOBATO*; SEBASTIAN P. RIUS; VALERIA R. TUROWSKI; PAULA CASATI; EDUARDO J. ZABALETA; DIEGO F. GOMEZ-CASATI; ALEJANDRO ARAYA

MOLECULAR PLANT

OXFORD UNIV PRESS

Lugar: Oxford; Año: 2011 vol. 4 p. 127 - 143

1674-2052

We characterized the transcriptomic response of transgenic plants carrying a mitochondrial dysfunction inducedby the expression of the unedited form of the ATP synthase subunit 9. The u-ATP9 transgene driven by A9 andAPETALA3 promoters induce mitochondrial dysfunction revealed by a decrease in both oxygen uptake and adenine nucleotides(ATP, ADP) levels without changes in the ATP/ADP ratio. Furthermore, we measured an increase in ROS accumulationand a decrease in glutathione and ascorbate levels with a concomitant oxidative stress response. The transcriptome analysisof young Arabidopsis flowers, validated by qRT?PCR and enzymatic or functional tests, showed dramatic changes inu-ATP9 plants. Both lines display a modification in the expression of various genes involved in carbon, lipid, and cell wallmetabolism, suggesting that an important metabolic readjustment occurs in plants with a mitochondrial dysfunction. Interestingly,transcript levels involved in mitochondrial respiration, protein synthesis, and degradation are affected. Moreover,the levels of several mRNAs encoding for transcription factors and DNA binding proteins were also changed. Some ofthem are involved in stress and hormone responses, suggesting that several signaling pathways overlap. Indeed, the transcriptomedata revealed that the mitochondrial dysfunction dramatically alters the expression of genes involved in signalingpathways, including those related to ethylene, absicic acid, and auxin signal transduction. Our data suggest that themitochondrial dysfunction model used in this report may be useful to uncover the retrograde signaling mechanism betweenthe nucleus and mitochondria in plant cells.