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  • 1
    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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    Paper (German National Licenses)
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  • 2
    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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    Paper (German National Licenses)
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  • 3
    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
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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