title: Comparison of intact Arabidopsis thaliana leaf transcript profiles during treatment with inhibitors of mitochondrial electron transport and TCA cycle.
abstract: Plant mitochondria signal to the nucleus leading to altered transcription of nuclear genes by a process called mitochondrial retrograde regulation (MRR). MRR is implicated in metabolic homeostasis and responses to stress conditions. Mitochondrial reactive oxygen species (mtROS) are a MRR signaling component, but whether all MRR requires ROS is not established. Inhibition of the cytochrome respiratory pathway by antimycin A (AA) or the TCA cycle by monofluoroacetate (MFA), each of which initiates MRR, can increase ROS production in some plant cells. We found that for AA and MFA applied to leaves of soil-grown Arabidopsis thaliana plants, ROS production increased with AA, but not with MFA, allowing comparison of transcript profiles under different ROS conditions during MRR. Variation in transcript accumulation over time for eight nuclear encoded mitochondrial protein genes suggested operation of both common and distinct signaling pathways between the two treatments. Consequences of mitochondrial perturbations for the whole transcriptome were examined by microarray analyses. Expression of 1316 and 606 genes was altered by AA and MFA, respectively. A subset of genes was similarly affected by both treatments, including genes encoding photosynthesis-related proteins. MFA treatment resulted in more down-regulation. Functional gene category (MapMan) and cluster analyses showed that genes with expression levels affected by perturbation from AA or MFA inhibition were most similarly affected by biotic stresses such as pathogens. Overall, the data provide further evidence for the presence of mtROS-independent MRR signaling, and support the proposed involvement of MRR and mitochondrial function in plant responses to biotic stress.
authors.affiliation: Department of Biology, Duke University, Durham, North Carolina, United States of America.
authors.forename: Ann L
authors.initials: AL
authors.lastname: Umbach
authors.forename: Jelena
authors.initials: J
authors.lastname: Zarkovic
authors.forename: Jianping
authors.initials: J
authors.lastname: Yu
authors.forename: Michael E
authors.initials: ME
authors.lastname: Ruckle
authors.forename: Lee
authors.initials: L
authors.lastname: McIntosh
authors.forename: Jeffery J
authors.initials: JJ
authors.lastname: Hock
authors.forename: Scott
authors.initials: S
authors.lastname: Bingham
authors.forename: Samuel J
authors.initials: SJ
authors.lastname: White
authors.forename: Rajani M
authors.initials: RM
authors.lastname: George
authors.forename: Chalivendra C
authors.initials: CC
authors.lastname: Subbaiah
authors.forename: David M
authors.initials: DM
authors.lastname: Rhoads
mesh_terms: D000968:Antimycin A / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects* / Q000235:genetics* / Q000378:metabolism; D002952:Citric Acid Cycle / Q000187:drug effects*; D004579:Electron Transport / Q000187:drug effects*; D005463:Fluoroacetates / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant / Q000187:drug effects*; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D018515:Plant Leaves / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D005463:Fluoroacetates; D017382:Reactive Oxygen Species; D000968:Antimycin A; C014815:fluoroacetic acid