scholarly journals Hyperactive recombination in the mitochondrial DNA of the natural death nuclear mutant of Neurospora crassa.

1993 ◽  
Vol 13 (11) ◽  
pp. 6778-6788 ◽  
Author(s):  
H Bertrand ◽  
Q Wu ◽  
B L Seidel-Rogol
Keyword(s):  
Mitochondrial Dna ◽  
Neurospora Crassa ◽  
Nuclear Gene ◽  
General System ◽  
Natural Death ◽  
Dna Restriction Fragments ◽  
Dna Restriction ◽  
Recessive Mutant ◽  
Nuclear Mutant ◽  
Mitochondrial Chromosome

In Neurospora crassa, a recessive mutant allele of a nuclear gene, nd (natural death), causes rapid degeneration of the mitochondrial DNA, a process that is manifested phenotypically as an accelerated form of senescence in growing and stationary mycelia. To examine the mechanisms that are involved in the degradation of the mitochondrial chromosome, several mitochondrial DNA restriction fragments unique to the natural-death mutant were cloned and characterized through restriction, hybridization, and nucleotide sequence analyses. All of the cloned DNA pieces contained one to four rearrangements that were generated by unequal crossing-over between direct repeats of several different nucleotide sequences that occur in pairs and are dispersed throughout the mitochondrial chromosome of wild-type Neurospora strains. The most abundant repeats, a family of GC-rich sequences that includes the so-called PstI palindromes, were not involved in the generation of deletions in the nd mutant. The implication of these results is that the nd allele hyperactivates a general system for homologous recombination in the mitochondria of N. crassa. Therefore, the nd+ allele either codes for a component of the complex of proteins that catalyzes recombination, and possibly repair and replication, of the mitochondrial chromosome or specifies a regulatory factor that controls the synthesis or activity of at least one enzyme or ancillary factor that is affiliated with mitochondrial DNA metabolism.

Hyperactive recombination in the mitochondrial DNA of the natural death nuclear mutant of Neurospora crassa

1993 ◽  
Vol 13 (11) ◽  
pp. 6778-6788
Author(s):  
H Bertrand ◽  
Q Wu ◽  
B L Seidel-Rogol
Keyword(s):  
Mitochondrial Dna ◽  
Neurospora Crassa ◽  
Nuclear Gene ◽  
General System ◽  
Natural Death ◽  
Dna Restriction Fragments ◽  
Dna Restriction ◽  
Recessive Mutant ◽  
Nuclear Mutant ◽  
Mitochondrial Chromosome

In Neurospora crassa, a recessive mutant allele of a nuclear gene, nd (natural death), causes rapid degeneration of the mitochondrial DNA, a process that is manifested phenotypically as an accelerated form of senescence in growing and stationary mycelia. To examine the mechanisms that are involved in the degradation of the mitochondrial chromosome, several mitochondrial DNA restriction fragments unique to the natural-death mutant were cloned and characterized through restriction, hybridization, and nucleotide sequence analyses. All of the cloned DNA pieces contained one to four rearrangements that were generated by unequal crossing-over between direct repeats of several different nucleotide sequences that occur in pairs and are dispersed throughout the mitochondrial chromosome of wild-type Neurospora strains. The most abundant repeats, a family of GC-rich sequences that includes the so-called PstI palindromes, were not involved in the generation of deletions in the nd mutant. The implication of these results is that the nd allele hyperactivates a general system for homologous recombination in the mitochondria of N. crassa. Therefore, the nd+ allele either codes for a component of the complex of proteins that catalyzes recombination, and possibly repair and replication, of the mitochondrial chromosome or specifies a regulatory factor that controls the synthesis or activity of at least one enzyme or ancillary factor that is affiliated with mitochondrial DNA metabolism.

Unstable mitochondrial DNA in natural-death nuclear mutants of Neurospora crassa

1989 ◽  
Vol 9 (10) ◽  
pp. 4259-4264
Author(s):  
B L Seidel-Rogol ◽  
J King ◽  
H Bertrand
Keyword(s):  
Neurospora Crassa ◽  
Mitochondrial Protein ◽  
Nuclear Gene ◽  
Recessive Mutation ◽  
Natural Death ◽  
Mitochondrial Ribosomes ◽  
Large Deletions ◽  
Group I ◽  
Mitochondrial Functions ◽  
Mitochondrial Chromosome

The natural-death mutant of Neurospora crassa has an accelerated senescence phenotype caused by a recessive mutation, nd, in a nuclear gene that is located in linkage group I. An examination of mitochondrial functions, however, revealed that the mutant has phenotypic and molecular defects similar to those commonly associated with maternally transmitted fungal senescence syndromes, including (i) deficiencies in cytochromes aa3 and b; (ii) a deficit in small subunits of mitochondrial ribosomes, and hence defective mitochondrial protein synthesis; and (iii) accumulation of gross rearrangements, including large deletions, in the mitochondrial chromosome of vegetatively propagated cells. These traits indicate that the nd+ allele codes for a function that is essential for stable maintenance of the mitochondrial chromosome, possibly a protein involved in replication, repair, or recombination.

scholarly journals Unstable mitochondrial DNA in natural-death nuclear mutants of Neurospora crassa.

1989 ◽  
Vol 9 (10) ◽  
pp. 4259-4264 ◽  
Author(s):  
B L Seidel-Rogol ◽  
J King ◽  
H Bertrand
Keyword(s):  
Neurospora Crassa ◽  
Mitochondrial Protein ◽  
Nuclear Gene ◽  
Recessive Mutation ◽  
Natural Death ◽  
Mitochondrial Ribosomes ◽  
Large Deletions ◽  
Group I ◽  
Mitochondrial Functions ◽  
Mitochondrial Chromosome

The natural-death mutant of Neurospora crassa has an accelerated senescence phenotype caused by a recessive mutation, nd, in a nuclear gene that is located in linkage group I. An examination of mitochondrial functions, however, revealed that the mutant has phenotypic and molecular defects similar to those commonly associated with maternally transmitted fungal senescence syndromes, including (i) deficiencies in cytochromes aa3 and b; (ii) a deficit in small subunits of mitochondrial ribosomes, and hence defective mitochondrial protein synthesis; and (iii) accumulation of gross rearrangements, including large deletions, in the mitochondrial chromosome of vegetatively propagated cells. These traits indicate that the nd+ allele codes for a function that is essential for stable maintenance of the mitochondrial chromosome, possibly a protein involved in replication, repair, or recombination.

Characterization of Cloned Mitochondrial DNA from the Teleost Fundulus heteroclitus and its Usefulness as an Interspecies Hybridization Probe

1986 ◽  
Vol 43 (10) ◽  
pp. 1866-1872 ◽  
Author(s):  
Lucia Irene González-Villaseñor ◽  
Amanda M. Burkhoff ◽  
Víctor Corces ◽  
Dennis A. Powers
Keyword(s):  
Mitochondrial Dna ◽  
Ethidium Bromide ◽  
Fundulus Heteroclitus ◽  
Staining Technique ◽  
Hybridization Probe ◽  
Cross Hybridization ◽  
Restriction Patterns ◽  
Ethidium Bromide Staining ◽  
Dna Restriction Fragments ◽  
Dna Restriction

Analysis of mitochondrial DNA endonuclease restriction patterns is a powerful tool for studying related species and variation within species. The ethidium bromide staining technique has limited the number of digestions of mitochondrial DNA per individual. Because 32P-end-labeling also imposes severe limitations, we have resorted to cloning the fish (Fundulus heteroclitus) mitochondrial genome in the lambda replacement vector EMBL-3. The clone was used as a radioactive probe via Southern blotting to detect mitochondrial DNA restriction fragments obtained by multiple restriction endonuclease digestions from small amounts of tissue. This technique offers much greater sensitivity than ethidium bromide staining. Moreover, it eliminates the expense and time to obtain highly purified mitochondrial DNA for the 32P-end-labeling procedure. It is also useful when the mtDNA is prepared from frozen tissue which has been a problem with the 32P-end-labeling technique. Because the cloned mitochondrial DNA has a high degree of cross-hybridization with the mitochondrial DNA of certain other fishes, it can be used to probe the mitochondrial DNA restriction patterns of a variety of fish species. However, its usefulness is restricted by the degree of relatedness to the species being cloned.

scholarly journals Molecular characterization of the mitochondrial DNA of a new stopper mutant ER-3 of Neurospora crassa.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 935-945
Author(s):  
A Almasan ◽  
N C Mishra
Keyword(s):  
Mitochondrial Dna ◽  
Neurospora Crassa ◽  
Molecular Level ◽  
Wild Type ◽  
Type Molecule ◽  
Nd5 Gene ◽  
Nucleotide Repeats ◽  
Two Populations ◽  
Mitochondrial Chromosome

Abstract An ethidium bromide-induced stopper mutant of Neurospora crassa is characterized at the molecular level. The mutant has two populations of mitochondrial DNA: a defective predominant mutant molecule and a basal level of the wild-type molecule. The aberrant DNA resulted after a 25-kbp deletion from the wild-type mitochondrial chromosome, which included major genes such as cytb, co1 and oli2. The deletion endpoints are located in the second intron of the ND5 gene, and in a sequence 250 nucleotides upstream of the co2 gene. The recombination has taken place between two nine nucleotide repeats CCCCGCCCC, one of which is close to a PstI palindrome at its 5' end. Thus the mutant ER-3 differs from all the other stopper mutants described previously in the extent and location of the deletions in the mtDNA.

scholarly journals Mutations in nuclear gene cyt-4 of Neurospora crassa result in pleiotropic defects in processing and splicing of mitochondrial RNAs.

Genetics ◽  
1989 ◽  
Vol 123 (1) ◽  
pp. 97-108 ◽  
Author(s):  
K F Dobinson ◽  
M Henderson ◽  
R L Kelley ◽  
R A Collins ◽  
A M Lambowitz
Keyword(s):  
Neurospora Crassa ◽  
Mitochondrial Protein ◽  
Nuclear Gene ◽  
Northern Hybridization ◽  
Rrna Gene ◽  
Mitochondrial Rna ◽  
Group I Introns ◽  
Group I ◽  
Processing Pathways ◽  
Aberrant Rna

Abstract The nuclear cyt-4 mutants of Neurospora crassa have been shown previously to be defective in splicing the group I intron in the mitochondrial large rRNA gene and in 3' end synthesis of the mitochondrial large rRNA. Here, Northern hybridization experiments show that the cyt-4-1 mutant has alterations in a number of mitochondrial RNA processing pathways, including those for cob, coI, coII and ATPase 6 mRNAs, as well as mitochondrial tRNAs. Defects in these pathways include inhibition of 5' and 3' end processing, accumulation of aberrant RNA species, and inhibition of splicing of both group I introns in the cob gene. The various defects in mitochondrial RNA synthesis in the cyt-4-1 mutant cannot be accounted for by deficiency of mitochondrial protein synthesis or energy metabolism, and they suggest that the cyt-4-1 mutant is defective in a component or components required for processing and/or turnover of a number of different mitochondrial RNAs. Defective splicing of the mitochondrial large rRNA intron in the cyt-4-1 mutant may be a secondary effect of failure to synthesize pre-rRNAs having the correct 3' end. However, a similar explanation cannot be invoked to account for defective splicing of the cob pre-mRNA introns, and the cyt-4-1 mutation may directly affect splicing of these introns.

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