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  • 1
    Electronic Resource
    Electronic Resource
    Alteration of the cytochrome c oxidase subunit 2 gene in the [exn-5] mutant of Neurospora crassa (1991)
    Springer
    Current genetics 20 (1991), S. 121-127 
    Details
    ISSN: 1432-0983
    Keywords: Neurospora ; Cytochrome c oxidase ; COXII ; Mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The maternally inherited [exn-5] mutant of Neurospora crassa is characterized by its slow-growth rate and deficiency of cytochrome aa 3 relative to wildtype strains. We have determined the DNA sequence of the COXI and COXII genes of the mutant, which encode subunits 1 and 2 of cytochrome c oxidase, respectively. No changes in the DNA sequence of the COXI gene relative to the corresponding wild-type gene were found. In the region of the COXII gene we found two alterations, one a C to T transition eight base pairs upstream of the coding sequence and the second within the coding sequence for subunit 2 affecting amino acid 27 of the precursor polypeptide (amino acid 15 of the mature polypeptide). The altered codon in [exn-5] specifies an isoleucine residue rather than the wild-type threonine residue. The corresponding position in subunit 2 sequences of all other organisms examined is conserved either as a threonine or a serine residue. Thus, we consider it likely that the mutation directly affecting the coding sequence of the polypeptide is responsible for the [exn-5] phenotype. Analysis of serially passaged heterokaryons constructed between wild-type and [exn-5] shows that both mutations segregate with the [exn-5] phenotype. Examination of mitochondrial translation products in [exn-5] revealed a deficiency of subunit 2, as well as the presence of a polypeptide that corresponds to a previously described precursor of subunit 1 that accumulates in a COXI mutant of N. crassa, [mi-3]. We propose possible relationships between [exn-5], [mi-3], and the nuclear su-1 [mi-3] allele, which suppresses both mutations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00312774
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  • 2
    Electronic Resource
    Electronic Resource
    Disruption of the gene encoding the 78-kilodalton subunit of the peripheral arm of complex I in Neurospora crassa by repeat induced point mutation (RIP) (1995)
    Springer
    Current genetics 27 (1995), S. 339-350 
    Details
    ISSN: 1432-0983
    Keywords: Neurospora ; Complex I ; RIP ; Mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We have used the procedure of sheltered RIP to generate mutants of the 78-kDa protein of the peripheral arm of Neurospora crassa complex I. The nuclei containing the mutations were initially isolated as one component of a heterokaryon but subsequent analysis showed that nuclei containing null alleles of the gene could be propagated as homokaryons. This demonstrates that the gene does not serve an essential function. Sequence analysis of one allele shows that 61 transition mutations were created resulting in 39 amino-acid changes including the introduction of four stop codons. Mutant strains grow at a slower rate than wild-type and exhibit a decrease in the production of conidia. Electron paramagnetic spectroscopy of mutant mitochondria suggest that they are deficient in Fe−S clusters N-1, N-3, and N-4.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00352103
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  • 3
    Electronic Resource
    Electronic Resource
    Inactivation of the Neurospora crassa mitochondrial outer membrane protein TOM70 by repeat-induced point mutation (RIP) causes defects in mitochondrial protein import and morphology (1999)
    Springer
    Current genetics 36 (1999), S. 137-146 
    Details
    ISSN: 1432-0983
    Keywords: Key wordsNeurospora ; TOM70 ; Mitochondria ; Protein import
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Mitochondrial biogenesis requires the efficient import of hundreds of different cytosolically translated preproteins into existing organelles. Recognition and translocation of preproteins at the mitochondrial outer membrane is achieved by the TOM complex (translocase of the outer mitochondrial membrane). The largest component of this complex is TOM70, an integral outer membrane protein with a large cytosolic domain thought to serve as a receptor for a specific group of preproteins. To investigate the functional role of TOM70 in Neurospora crassa the tom70 gene was inactivated using the natural phenomenon of repeat-induced point mutation (RIP). Mutant strains were identified that harbored RIPed tom70 alleles and contained no immunologically detectable TOM70. Strains that lack TOM70 grow more slowly than wild-type strains, conidiate poorly, and contain enlarged mitochondria. In vitro preprotein import studies using TOM70-deficient mitochondria revealed a defect in the uptake of the ADP/ATP carrier. Other preproteins tested were imported at wild-type rates with the exception of the precursor of the mitochondrial-processing peptidase (MPP) which was imported more efficiently by TOM70-deficient mitochondria. These data support the view that TOM70 plays a role as a specific receptor for carrier proteins in mitochondrial-preprotein import. The presence of tetratricopeptide repeats (TPRs) in the TOM70 sequence and the enlarged shape of mitochondria lacking TOM70 raise the possibility that the protein also plays a role in the maintenance of mitochondrial morphology.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050483
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  • 4
    Electronic Resource
    Electronic Resource
    Mutations in the structural gene for cytochrome c result in deficiency of both cytochromes aa 3 and c in Neurospora crassa (1994)
    Springer
    Current genetics 26 (1994), S. 329-335 
    Details
    ISSN: 1432-0983
    Keywords: Cytochrome c ; Cytochrome aa 3 ; Mitochondria ; Neurospora crassa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The cyt-12-12 mutant of Neurospora crassa is characterized by slow growth and a deficiency of spectrophotometrically-detectable cytochromes aa 3 and c. Using a sib-selection procedure we have isolated the cyt-12 + allele from a cosmid library of N. crassa genomic DNA. Characterization of the cyt-12 + allele reveals that it encodes the structural gene for cytochrome c. DNA sequence analysis of the cyt-12-12 allele revealed a mutation in the cytochrome c coding sequence that results in replacement of a glycine residue, which is invariant in the cytochrome c of other species, with an aspartic acid. Genetic analysis confirms that cyt-12-12 is allelic with the previously-characterized cyc-1-1 mutant, which was also shown to affect the single locus encoding cytochrome c in N. crassa. We suggest that the amount of functional cytochrome c present in mitochondria influences the level of cytochrome aa 3 .
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310497
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  • 5
    Electronic Resource
    Electronic Resource
    Disruption of the nuclear gene encoding the 20.8-kDa subunit of NADH:ubiquinone reductase of Neurospora mitochondria (1996)
    Springer
    Molecular genetics and genomics 252 (1996), S. 177-183 
    Details
    ISSN: 1617-4623
    Keywords: Key wordsNeurospora crassa ; Mitochondria ; Complex I ; Assembly ; Gene disruption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The nuclear gene coding for the 20.8k-kDa subunit of the membrane arm of respiratory chain NADH:ubiquinone reductase (Complex I) from Neurospora crassa, nuo-20.8 was localized on linkage group I of the fungal genome. A genomic DNA fragment containing this gene was cloned and a duplication was created in a strain of N. crassa by transformation. To generate RIP (repeat-induced point) mutations in the duplicated sequence, the transformant was crossed with another strain carrying an auxotrophic marker on chromosome I. To increase the chance of finding an isolate with a non-functional nuo-20.8 gene, random progeny from the cross were selected against this auxotrophy since RIP of the target gene will only occur in the nucleus carrying the duplication. Among these, we isolated and characterised a mutant strain that lacks the 20.8 kDa mitochondrial protein, indicating that this cysteine-rich polypeptide is not essential. Nevertheless, the absence of the 20.8-kDa subunit prevents the full assembly of complex I. It appears that the peripheral arm and two intermediates of the membrane arm of the enzyme are still formed in the mutant mitochondria. The NADH:ubiquinone reductase activity of sonicated mitochondria from the mutant is rotenone insensitive. Electron microscopy of mutant mitochondria does not reveal any alteration in the structure or numbers of the organelles.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004389670020
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  • 6
    Electronic Resource
    Electronic Resource
    Comparative study of rest technetium-99m sestamibi SPET and low-dose dobutamine stress echocardiography for the early assessment of myocardial viability after acute myocardial infarction: importance of the severity of the infarct-related stenosis (1996)
    Springer
    European journal of nuclear medicine 23 (1996), S. 748-755 
    Details
    ISSN: 1619-7089
    Keywords: Myocardial infarction ; Technetium-99m sestamibi ; Dobutamine stress echocardiography ; Coronary anatomy ; Viability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rest technetium-99m sestamibi single-photon emission tomography (SPET) has been shown to under-estimate viability in some patients with chronic ischaemic myocardial dysfunction. The present study was designed to appraise the value of99mTc-sestamibi as a viability tracer in patients with a recent myocardial infarction and to determine factors that might influence its accuracy in assessing infarct size. Therefore, rest99mTc-sestamibi SPET, low-dose dobutamines stress echocardiography and quantitative coronary angiography were performed in 51 patients with a recent myocardial infarction. Perfusion activity and regional wall motion were scored semi-quantitatively using the same segmental division of the left ventricle. Assessment of99mTc-sestamibi uptake as a marker of viability was performed by comparing a binary uptake score (viable=〉50% vs necrotic =≤50% of the maximal tracer activity) with a binary wall motion classification during low-dose dobutamine infusion (viable=normal/hypokinetic vs necrotic=akinetic/dyskinetic). Infarct size, expressed as the number of segments with evidence of necrotic tissue, was significantly greater in the scintigraphic study than in the echocardiographic study (2.8±1.5 vs 2.2±1.3,P=0.006). This overestimation of infarct size by99mTc-sestamibi was present only in patients with a severe infarct-related stenosis (% diameter stenosis ≽65%–100%) and particularly those with “late” reperfusion therapy (time delay ≽180 min). In patients without a severe infarct-related stenosis,99mTc-sestamibi was able to accurately distinguish viable from necrotic segments. Thus, rest99mTc-sestamibi scintigraphy early after acute myocardial infarction may underestimate residual viability within the infarct region, particularly in patients with low flow state coronary anatomy, as a result of a severe infarct-related stenosis and/or late reperfusion therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00843702
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  • 7
    Electronic Resource
    Electronic Resource
    Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction (1997)
    Springer
    European journal of nuclear medicine 24 (1997), S. 1121-1127 
    Details
    ISSN: 1619-7089
    Keywords: Jeopardized myocardium ; Adenosine ; Technetium-99m sestamibi ; Stenosis severity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study investigated the value of technetium-99m sestarnibi scintigraphy in identifying patients at risk for post-infarct ischaemia (=jeopardized myocardium), especially within the reperfused infarct region. In 51 patients with a recent (〈I month) myocardial infarction, adenosine99mTc-sestamibi single-photon emission tomography (SPET) and dobutamine stress echocardiography (DSE) were performed and correlated with the presence of significant coronary artery stenosis [% diameter stenosis (DS) 〉50%] on quantitative coronary angiography. Regional perfusion activity was analysed semiquantitatively (score 0–4) on a 13-segment left ventricular model. DSE was used for the estimation of the infarct size (low-dose DSE) and for concomitant evaluation of ischaemia (high-dose DSE). A reversible perfusion defect within the infarct region was observed in 20 of the 37 patients with a significant infarct-related lesion (sensitivity of 54%) and only in one patient without a significant infarct-related lesion (specificity of 93%). Further analysis revealed that the scintigraphic assessment of jeopardized myocardium was fairly good in patients with a moderate (DS 51%–64%) infarct-related stenosis but was inadequate in patients with a severe (DS≥65%) infarct-related stenosis (sensitivity of 80% vs 36%,P〈0.01), while the echocardiographic detection of ischaemia was not influenced by stenosis severity (sensitivity of 73% in both subgroups). This scintigraphic under-estimation of jeopardized myocardium was mainly related to a severely impaired myocardial perfusion under baseline conditions, as was evidenced by a significantly more severe rest perfusion score in the infarct region in patients with a severe stenosis as compared to those with a moderate stenosis (average score: 1.5±0.7 vs 2.1±0.6,P〈0.01), while infarct size on echocardiography was similar for both subgroups. It may be concluded that early after an acute myocardial infarction, adenosine99mTc-sestamibi SPET may underestimate reperfused but still jeopardized myocardium, particularly in patients with a severe infarct-related stenosis. In these patients the evaluation of the ischaemic burden on rest-stress scintigraphy is hampered by the presence of a severely impaired myocardial perfusion in resting conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01254243
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  • 8
    Electronic Resource
    Electronic Resource
    Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction (1997)
    Springer
    European journal of nuclear medicine 24 (1997), S. 1121-1127 
    Details
    ISSN: 1619-7089
    Keywords: Key words: Jeopardized myocardium ; Adenosine ; Technetium-99m sestamibi ; Stenosis severity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. This study investigated the value of technetium-99m sestamibi scintigraphy in identifying patients at risk for post-infarct ischaemia (=jeopardized myocardium), especially within the reperfused infarct region. In 51 patients with a recent (〈1 month) myocardial infarction, adenosine 99mTc-sestamibi single-photon emission tomography (SPET) and dobutamine stress echocardiography (DSE) were performed and correlated with the presence of significant coronary artery stenosis [% diameter stenosis (DS) 〉50%] on quantitative coronary angiography. Regional perfusion activity was analysed semi-quantitatively (score 0–4) on a 13-segment left ventricular model. DSE was used for the estimation of the infarct size (low-dose DSE) and for concomitant evaluation of ischaemia (high-dose DSE). A reversible perfusion defect within the infarct region was observed in 20 of the 37 patients with a significant infarct-related lesion (sensitivity of 54%) and only in one patient without a significant infarct-related lesion (specificity of 93%). Further analysis revealed that the scintigraphic assessment of jeopardized myocardium was fairly good in patients with a moderate (DS 51%–64%) infarct-related stenosis but was inadequate in patients with a severe (DS≥65%) infarct-related stenosis (sensitivity of 80% vs 36%, P〈0.01), while the echocardiographic detection of ischaemia was not influenced by stenosis severity (sensitivity of 73% in both subgroups). This scintigraphic underestimation of jeopardized myocardium was mainly related to a severely impaired myocardial perfusion under baseline conditions, as was evidenced by a significantly more severe rest perfusion score in the infarct region in patients with a severe stenosis as compared to those with a moderate stenosis (average score: 1.5±0.7 vs 2.1±0.6, P〈0.01), while infarct size on echocardiography was similar for both subgroups. It may be concluded that early after an acute myocardial infarction, adenosine 99mTc-sestamibi SPET may underestimate reperfused but still jeopardized myocardium, particularly in patients with a severe infarct-related stenosis. In these patients the evaluation of the ischaemic burden on rest-stress scintigraphy is hampered by the presence of a severely impaired myocardial perfusion in resting conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01254243
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