Variability in the Echinococcus granulosus Cytochrome C oxidase 1 mitochondrial gene sequence from livestock in Turkey and a re-appraisal of the G1–3 genotype cluster

Isostenosmylus Krüger, 1913 is the richest genus of Osmylidae of the Neotropical region, with 17 described species so far, which are distributed mainly in the Andean region and in the South of Brazil and Paraguay. A new remarkable Colombian species of Isostenosmylus—I. ammirabilis sp. nov.—is herein described and illustrated. DNA barcode of mitochondrial gene cytochrome c oxidase subunit I (COI) for this species is also provided. Taxonomic keys for the genus are updated.

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Mitochondrial Antisense RNA for Cytochrome C Oxidase (MARCO) Can Induce Morphologic Changes and Cell Death in Human Hematopoietic Cell Lines

Blood ◽

10.1182/blood.v90.11.4567.4567_4567_4577 ◽

1997 ◽

Vol 90 (11) ◽

pp. 4567-4577 ◽

Cited By ~ 2

Author(s):

Naoki Shirafuji ◽

Satoshi Takahashi ◽

Satoru Matsuda ◽

Shigetaka Asano

Keyword(s):

Molecular Weight ◽

Cell Death ◽

Cytochrome C ◽

Cytochrome C Oxidase ◽

Antisense Rna ◽

Mitochondrial Gene ◽

Neutrophilic Granulocytes ◽

High Molecular Weight Dna ◽

Tnf Α ◽

Morphologic Changes

To identify essential molecules capable of inducing terminal morphologic maturation and cell death of myeloid progenitor cells, we isolated cDNA clones by functional expression cloning using a library constructed from all-trans retinoic acid (ATRA)-treated human promyelocytic HL-60 cells. Clones which induced morphologic changes in HL-60 cells from blastic cells to mature neutrophilic granulocytes were selected. The isolated positive cDNA clone was demonstrated to encode an antisense RNA for cytochrome c oxidase/serine tRNA derived from a mitochondrial gene (MARCO). When MARCO was expressed in HL-60 cells with the lac switch system, blastic cell morphology became neutrophilic after 48-hour incubation with IPTG, and cell death was observed after 3 days. Also, high molecular weight DNA fragmentation was observed after 36 hours in culture. Similar results were observed using transformants from human K562 cells and CMK cells. RT-PCR analysis revealed that MARCO was transcribed in both ATRA and TNF-α systems, and also in human blood neutrophilic granulocytes. Following transfection with cytochrome c oxidase expression plasmids, TNF-α–induced high molecular weight DNA fragmentation in U937 cells and HL-60 cells was inhibited in these transformants. These results indicate that maturational changes in hematopoietic cells and the process of cell death may be induced by mitochondrial respiratory insufficiency, and also that the mitochondrial gene MARCO may be used as one of the candidates for gene supplementation therapy for the acute leukemias.

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The maize cytochrome c oxidase subunit I gene: sequence, expression and rearrangement in cytoplasmic male sterile plants

The EMBO Journal ◽

10.1002/j.1460-2075.1985.tb03828.x ◽

1985 ◽

Vol 4 (7) ◽

pp. 1617-1623 ◽

Cited By ~ 135

Author(s):

Peter G. Isaac ◽

Valerie P. Jones ◽

Christopher J. Leaver

Keyword(s):

Cytochrome C ◽

Cytochrome C Oxidase ◽

Gene Sequence ◽

Male Sterile ◽

Cytoplasmic Male Sterile ◽

Oxidase Subunit ◽

I Gene

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Using DNA barcodes to assess identity and diversity of Dendropsophus minutus: Failure?

Zootaxa ◽

10.11646/zootaxa.1691.1.3 ◽

2008 ◽

Vol 1691 (1) ◽

pp. 67 ◽

Cited By ~ 3

Author(s):

M. ALEX SMITH

Keyword(s):

Cytochrome C ◽

Small Group ◽

Cytochrome C Oxidase ◽

Species Identification ◽

Mitochondrial Gene ◽

Dna Barcode ◽

Gene Region ◽

Dna Barcodes ◽

Taxonomic Groups

The 5' end (Folmer or Barcode region) of cytochrome c oxidase 1 (CO1) has been proposed as the gene region of choice for a standardized animal DNA barcode (Hebert et al. 2003). Concerns have been raised regarding the decision to utilize this particular mitochondrial gene region as a barcode. Nevertheless, widely divergent taxonomic groups have reported success using CO1 for both species identification and discovery. The utility of CO1 for barcoding amphibians was raised early on (Vences, et al. 2005) and concerns for this group were reported widely (Waugh 2007)—although some considered that the reporting of the concerns outstripped the data that had been analyzed at that point (Smith et al. 2008). Indeed, our analysis of CO1 for a small group of Holarctic amphibians was neither more difficult to generate nor to analyze than for other groups where we have utilized the technique.

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Mitochondrial DNA replication and transcription are dissociated during embryonic cardiac hypertrophy

AJP Cell Physiology ◽

10.1152/ajpcell.1991.261.6.c1091 ◽

1991 ◽

Vol 261 (6) ◽

pp. C1091-C1098 ◽

Cited By ~ 7

Author(s):

J. M. Kennedy ◽

S. R. Lobacz ◽

S. W. Kelley

Keyword(s):

Mitochondrial Dna ◽

Cytochrome C ◽

Cardiac Hypertrophy ◽

Cytochrome C Oxidase ◽

Oxidase Activity ◽

Citrate Synthase ◽

Incubation Temperature ◽

Mitochondrial Gene ◽

Gene Replication ◽

Mitochondrial Dna Copy Number

Cardiac hypertrophy was produced in embryonic chicks by decreasing the incubation temperature from 38 degrees C to 32 degrees C on day 11. Increases in ventricular protein, RNA, and DNA support the cardiac enlargement. Cytochrome-c oxidase activity and citrate synthase activity were depressed in hypothermic ventricles by 63% and 56%, respectively. No significant differences were seen in enzyme activities in pectoralis muscles. The involvement of mitochondrial gene replication and transcription was evaluated using a cDNA clone for the mitochondrially encoded subunit III of cytochrome-c oxidase (CO III). Quantitative slot-blot analysis demonstrated that the relative CO III mRNA concentration was reduced in hypothermic ventricles. In contrast, the relative mitochondrial DNA concentration was increased in hypothermic ventricles. Taken together, these data indicate that a hypothermia-induced decrease in cytochrome-c oxidase activity is associated with a decrease in CO III mRNA, which is not coupled to a decrease in the mitochondrial DNA copy number. This dissociation of mitochondrial gene replication and transcription may provide a useful model for examining the regulation of mitochondrial biogenesis.

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Cytochrome c oxidase III as a mechanism for apoptosis in heart failure following myocardial infarction

AJP Cell Physiology ◽

10.1152/ajpcell.00045.2009 ◽

2009 ◽

Vol 297 (4) ◽

pp. C928-C934 ◽

Cited By ~ 23

Author(s):

Changgong Wu ◽

Lin Yan ◽

Christophe Depre ◽

Sunil K. Dhar ◽

You-Tang Shen ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Heart Failure ◽

Cytochrome C ◽

Protein Expression ◽

Cell Viability ◽

Cytochrome C Oxidase ◽

Mitochondrial Gene

Cytochrome c oxidase (COX) is composed of 13 subunits, of which COX I, II, and III are encoded by a mitochondrial gene. COX I and II function as the main catalytic components, but the function of COX III is unclear. Because myocardial ischemia affects mitochondrial oxidative metabolism, we hypothesized that COX activity and expression would be affected during postischemic cardiomyopathy. This hypothesis was tested in a monkey model following myocardial infarction (MI) and subsequent pacing-induced heart failure (HF). In this model, COX I protein expression was decreased threefold after MI and fourfold after HF ( P < 0.05 vs. sham), whereas COX II expression remained unchanged. COX III protein expression increased 5-fold after MI and further increased 10-fold after HF compared with sham ( P < 0.05 vs. sham). The physiological impact of COX III regulation was examined in vitro. Overexpression of COX III in mitochondria of HL-1 cells resulted in an 80% decrease in COX I, 60% decrease in global COX activity, 60% decrease in cell viability, and threefold increase in apoptosis ( P < 0.05). Oxidative stress induced by H2O2 significantly ( P < 0.05) increased COX III expression. H2O2 decreased cell viability by 47 ± 3% upon overexpression of COX III, but only by 12 ± 5% in control conditions ( P < 0.05). We conclude that ischemic stress in vivo and oxidative stress in vitro lead to upregulation of COX III, followed by downregulation of COX I expression, impaired COX oxidative activity, and increased apoptosis. Therefore, upregulation of COX III may contribute to the increased susceptibility to apoptosis following MI and subsequent HF.

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DNA barcodes for insect pest identification: a test case with tussock moths (Lepidoptera: Lymantriidae)

Canadian Journal of Forest Research ◽

10.1139/x05-276 ◽

2006 ◽

Vol 36 (2) ◽

pp. 337-350 ◽

Cited By ~ 106

Author(s):

Shelley L Ball ◽

Karen F Armstrong

Keyword(s):

Cytochrome C ◽

Cytochrome C Oxidase ◽

Sequence Data ◽

Mitochondrial Gene ◽

Insect Pest ◽

Reference Sequence ◽

Identification System ◽

Pest Species ◽

Dna Barcodes ◽

Data Set

Reliable and rapid identification of exotic pest species is critical to biosecurity. However, identification of morphologically indistinct specimens, such as immature life stages, that are frequently intercepted at borders is often impossible. Several DNA-based methods have been used for species identification; however, a more universal and anticipatory identification system is needed. Consequently, we tested the ability of DNA "barcodes" to identify species of tussock moths (Lymantriidae), a family containing several important pest species. We sequenced a 617 base pair fragment of the mitochondrial gene cytochrome c oxidase 1 for 20 lymantriid species. We used these, together with other Noctuoidea species sequences from GenBank and the Barcoding of Life Database to create a "profile" or reference sequence data set. We then tested the ability of this profile to provide correct species identifications for 93 additional lymantriid specimens from a data set of mock unknowns. Of the unknowns, 100% were correctly identified by the cytochrome c oxidase 1 profile. Mean interspecific sequence (Kimura 2-parameter) divergence was an order of magnitude greater (14%) than mean intraspecific divergence (<1%). Four species showed deeper genetic divergences among populations. We conclude that DNA barcodes provide a highly accurate means of identifying lymantriid species and show considerable promise as a universal approach to DNA-based identification of pest insects.

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Mitochondrial Antisense RNA for Cytochrome C Oxidase (MARCO) Can Induce Morphologic Changes and Cell Death in Human Hematopoietic Cell Lines

Blood ◽

10.1182/blood.v90.11.4567 ◽

1997 ◽

Vol 90 (11) ◽

pp. 4567-4577 ◽

Cited By ~ 21

Author(s):

Naoki Shirafuji ◽

Satoshi Takahashi ◽

Satoru Matsuda ◽

Shigetaka Asano

Keyword(s):

Molecular Weight ◽

Cell Death ◽

Cytochrome C ◽

Cytochrome C Oxidase ◽

Antisense Rna ◽

Mitochondrial Gene ◽

Neutrophilic Granulocytes ◽

High Molecular Weight Dna ◽

Tnf Α ◽

Morphologic Changes

Abstract To identify essential molecules capable of inducing terminal morphologic maturation and cell death of myeloid progenitor cells, we isolated cDNA clones by functional expression cloning using a library constructed from all-trans retinoic acid (ATRA)-treated human promyelocytic HL-60 cells. Clones which induced morphologic changes in HL-60 cells from blastic cells to mature neutrophilic granulocytes were selected. The isolated positive cDNA clone was demonstrated to encode an antisense RNA for cytochrome c oxidase/serine tRNA derived from a mitochondrial gene (MARCO). When MARCO was expressed in HL-60 cells with the lac switch system, blastic cell morphology became neutrophilic after 48-hour incubation with IPTG, and cell death was observed after 3 days. Also, high molecular weight DNA fragmentation was observed after 36 hours in culture. Similar results were observed using transformants from human K562 cells and CMK cells. RT-PCR analysis revealed that MARCO was transcribed in both ATRA and TNF-α systems, and also in human blood neutrophilic granulocytes. Following transfection with cytochrome c oxidase expression plasmids, TNF-α–induced high molecular weight DNA fragmentation in U937 cells and HL-60 cells was inhibited in these transformants. These results indicate that maturational changes in hematopoietic cells and the process of cell death may be induced by mitochondrial respiratory insufficiency, and also that the mitochondrial gene MARCO may be used as one of the candidates for gene supplementation therapy for the acute leukemias.

Download Full-text