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Evidence of mitochondrial involvement in the transduction of signals required for the induction of genes associated with pathogen attack and senescence
Author(s) -
Maxwell Denis P.,
Nickels Roxy,
McIntosh Lee
Publication year - 2002
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2002.01216.x
Subject(s) - biology , alternative oxidase , mitochondrion , nicotiana tabacum , microbiology and biotechnology , programmed cell death , intracellular , senescence , gene , antimycin a , mitochondrial permeability transition pore , gene expression , retrograde signaling , biochemistry , apoptosis
Summary 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 H 2 O 2 and salicylic acid (SA). AA, H 2 O 2 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 H 2 O 2 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, H 2 O 2 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.