Mitochondrial complex I in the network of known and unknown facts

Chomová, Mária; Račay, Peter

doi:10.4149/gpb_2010_01_3

Cited by 12 publications

(10 citation statements)

References 51 publications

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“…These observations correspond well with our study, as we observed effects on the oxidative phosphorylation pathway and on the mitochondrial dysfunction pathway (Table 2). The dysfunctioning of mitochondria - and more specifically complex I to which the NADH:ubiquinone oxidoreductase paralogous gene family belongs (Table 3) - is often associated with generation of reactive oxygen species as well as the activation of the mitochondrial apoptosis-inducing pathway (56). Although induced apoptosis in mitochondria is often associated with microcystin exposure in a variety of species (46, 47), we observed down-regulated apoptosis inducing factors; i.e.…”

Section: Discussionmentioning

confidence: 99%

Identification of Pathways, Gene Networks, and Paralogous Gene Families in Daphnia pulex Responding to Exposure to the Toxic Cyanobacterium Microcystis aeruginosa

Asselman

Coninck

Colbourne³

et al. 2012

Environ. Sci. Technol.

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Although cyanobacteria produce a wide range of natural toxins that impact aquatic organisms, food webs, and water quality, the mechanisms of toxicity are still insufficiently understood. Here, we implemented a whole-genome expression microarray to identify pathways, gene networks, and paralogous gene families responsive to Microcystis stress in Daphnia pulex. Therefore, neonates of a sensitive isolate were given a diet contaminated with Microcystis to contrast with those given a control diet for 16 days. The microarray revealed 2247 differentially expressed (DE) genes (7.6% of the array) in response to Microcystis, of which 17% are lineage-specific (i.e., these genes have no detectable homology to any other gene in currently available databases) and 49% are gene duplicates (paralogues). We identified four pathways/gene networks and eight paralogous gene families affected by Microcystis. Differential regulation of the ribosome, including three paralogous gene families encoding 40S, 60S, and mitochondrial ribosomal proteins, suggests an impact of Microcystis on protein synthesis of D. pulex. In addition, differential regulation of the oxidative phosphorylation pathway (including the NADH:ubquinone oxidoreductase gene family) and the trypsin paralogous gene family (a major component of the digestive system in D. pulex) could explain why fitness is reduced based on energy budget considerations.

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Section: Discussionmentioning

confidence: 99%

Identification of Pathways, Gene Networks, and Paralogous Gene Families in Daphnia pulex Responding to Exposure to the Toxic Cyanobacterium Microcystis aeruginosa

Asselman

Coninck

Colbourne³

et al. 2012

Environ. Sci. Technol.

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“…The possible effects of a reduction on the mitochondrial Complex I activity are different and complex [62], including increased ROS production [63], increased apoptosis [64], reduced ATP synthesis [65], and even alterations on innate immunity [66]. Interestingly, all these effects have been already reported in CF cells [12], [67], [68], [69], [70], [71].…”

Section: Discussionmentioning

confidence: 99%

The Mitochondrial Complex I Activity Is Reduced in Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function

et al. 2012

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Cystic fibrosis (CF) is a frequent and lethal autosomal recessive disease. It results from different possible mutations in the CFTR gene, which encodes the CFTR chloride channel. We have previously studied the differential expression of genes in CF and CF corrected cell lines, and found a reduced expression of MTND4 in CF cells. MTND4 is a mitochondrial gene encoding the MTND4 subunit of the mitochondrial Complex I (mCx-I). Since this subunit is essential for the assembly and activity of mCx-I, we have now studied whether the activity of this complex was also affected in CF cells. By using Blue Native-PAGE, the in-gel activity (IGA) of the mCx-I was found reduced in CFDE and IB3-1 cells (CF cell lines) compared with CFDE/6RepCFTR and S9 cells, respectively (CFDE and IB3-1 cells ectopically expressing wild-type CFTR). Moreover, colon carcinoma T84 and Caco-2 cells, which express wt-CFTR, either treated with CFTR inhibitors (glibenclamide, CFTR(inh)-172 or GlyH101) or transfected with a CFTR-specific shRNAi, showed a significant reduction on the IGA of mCx-I. The reduction of the mCx-I activity caused by CFTR inhibition under physiological or pathological conditions may have a profound impact on mitochondrial functions of CF and non-CF cells.

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“…Pathogens, such as Helicobacter pylori, have been shown to require similar reductases to withstand oxidative stress while inside phagocytic cells [77]. Alternatively, there is speculation that deregulation of NADH may be involved in eukaryotic programmed cell death, suggesting a pathogenic mechanism for this protein [78], [79]. Further research examining these discrete protein interactions will better elucidate the specific T6SS pathogenesis mechanisms.…”

Section: Discussionmentioning

confidence: 99%

A Type VI Secretion System Encoding Locus Is Required for Bordetella bronchiseptica Immunomodulation and Persistence In Vivo

et al. 2012

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Type VI Secretion Systems (T6SSs) have been identified in numerous Gram-negative pathogens, but the lack of a natural host infection model has limited analysis of T6SS contributions to infection and pathogenesis. Here, we describe disruption of a gene within locus encoding a putative T6SS in Bordetella bronchiseptica strain RB50, a respiratory pathogen that circulates in a broad range of mammals, including humans, domestic animals, and mice. The 26 gene locus encoding the B. bronchiseptica T6SS contains apparent orthologs to all known core genes and possesses thirteen novel genes. By generating an in frame deletion of clpV, which encodes a putative ATPase required for some T6SS-dependent protein secretion, we observe that ClpV contributes to in vitro macrophage cytotoxicity while inducing several eukaryotic proteins associated with apoptosis. Additionally, ClpV is required for induction of IL-1β, IL-6, IL-17, and IL-10 production in J774 macrophages infected with RB50. During infections in wild type mice, we determined that ClpV contributes to altered cytokine production, increased pathology, delayed lower respiratory tract clearance, and long term nasal cavity persistence. Together, these results reveal a natural host infection system in which to interrogate T6SS contributions to immunomodulation and pathogenesis.

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Mitochondrial complex I in the network of known and unknown facts

Cited by 12 publications

References 51 publications

Identification of Pathways, Gene Networks, and Paralogous Gene Families in Daphnia pulex Responding to Exposure to the Toxic Cyanobacterium Microcystis aeruginosa

Identification of Pathways, Gene Networks, and Paralogous Gene Families in Daphnia pulex Responding to Exposure to the Toxic Cyanobacterium Microcystis aeruginosa

The Mitochondrial Complex I Activity Is Reduced in Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function

A Type VI Secretion System Encoding Locus Is Required for Bordetella bronchiseptica Immunomodulation and Persistence In Vivo

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