Evidence of mitochondrial involvement in the transduction of signals required for the induction of genes associated with pathogen attack and senescence.
Using the mRNA differential display technique, seven cDNAs have been isolated that are rapidly induced when cultured tobacco (Nicotiana tabacum) cells are treated with the mitochondrial electron transport inhibitor antimycin A (AA). Interestingly, six of the cDNAs show distinct similarity to genes known to be induced by processes that involve programmed cell death (PCD), such as senescence and pathogen attack. All of the cDNAs as well as Aox1, a gene encoding the alternative oxidase, were found to also be strongly induced by H2O2 and salicylic acid (SA). AA, H2O2 and SA treatment of tobacco cells caused a rapid rise in intracellular ROS accumulation that, when prevented by antioxidant treatment, resulted in inhibition of gene induction. Besides AA, both H2O2 and SA were found to disrupt normal mitochondrial function resulting in decreased rates of electron transport and a lowering of cellular ATP levels. Furthermore, the pre-treatment of tobacco cells with bongkrekic acid, a known inhibitor of the mitochondrial permeability transition pore in animal cells, was found to completely block gene induction when AA, H2O2 or SA were subsequently added. These findings suggest that the mitochondrion may serve an important role in conveying intracellular stress signals to the nucleus, leading to alterations in gene expression.
Maxwell
Denis P
DP
Michigan State University-Department of Energy Plant Research Laboratory, Michigan State University, East Lansing 48824, USA.
Nickels
Roxy
R
McIntosh
Lee
L
D000255:Adenosine Triphosphate / Q000378:metabolism; D000968:Antimycin A / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D001865:Bongkrekic Acid / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects / Q000502:physiology; D019069:Cell Respiration / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D003001:Cloning, Molecular; D018076:DNA, Complementary / Q000737:chemistry / Q000235:genetics / Q000302:isolation & purification; D004579:Electron Transport / Q000187:drug effects; D020869:Gene Expression Profiling; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D017343:Genes, Plant / Q000235:genetics*; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007700:Kinetics; D008928:Mitochondria / Q000502:physiology*; D024101:Mitochondrial Proteins; D008969:Molecular Sequence Data; D010088:Oxidoreductases / Q000096:biosynthesis; D010940:Plant Proteins; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D020156:Salicylic Acid / Q000494:pharmacology; D017422:Sequence Analysis, DNA; D015398:Signal Transduction / Q000502:physiology*; D014026:Nicotiana / Q000166:cytology / Q000235:genetics / Q000378:metabolism; D015533:Transcriptional Activation; D000099188:Alternative Oxidase
D000255:Adenosine Triphosphate; D000968:Antimycin A; D000975:Antioxidants; D001865:Bongkrekic Acid; D018076:DNA, Complementary; D006861:Hydrogen Peroxide; D024101:Mitochondrial Proteins; D010088:Oxidoreductases; D010940:Plant Proteins; D017382:Reactive Oxygen Species; D020156:Salicylic Acid; D000099188:Alternative Oxidase