Plasmids of Eukaryotes

Esser, Karl; Kück, Ulrich; Lang-Hinrichs, Christine; Lemke, Paul A.; Osiewacz, Heinz D.; Ståhl, Ulf; Tudzynski, Paul

doi:10.1007/978-3-642-82585-9

Cited by 84 publications

(14 citation statements)

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“…In Neurospora, Podospora, and Aspergillus, senescence is invariably characterized by a progressive deterioration of mitochondrial function, including the disappearance of cytochromes a and b and accumulation of rearranged mitochondrial chromosomes (mtDNA) during vegetative growth and asexual spore formation (reviewed by Bertrand 1983Bertrand , 1986Esser et al 1986). The genetic factors that determine the predisposition to senescence, as well as the 'Author to whom all correspondence should be addressed.…”

Section: Introductionmentioning

confidence: 99%

“…Senescence, a process of clonal deterioration leading to death, occurs regularly in a number of filamentous fungi, including Podospora (Marcou 196 1 ;Esser et al 1986), Aspergillus (Mather and Jinks 1958;Caten 1972), Pestalozzia (Chevaugeon and Lefort 1960;Chevaugeon and Digbeau 1960), Helminthosporium (Lindberg 1959), and Neurospora (Bertrand et al 1968;Bertrand and Pittenger 1969;Rieck et al 1982;Bertrand 1983). In Neurospora, Podospora, and Aspergillus, senescence is invariably characterized by a progressive deterioration of mitochondrial function, including the disappearance of cytochromes a and b and accumulation of rearranged mitochondrial chromosomes (mtDNA) during vegetative growth and asexual spore formation (reviewed by Bertrand 1983Bertrand , 1986Esser et al 1986).…”

Section: Introductionmentioning

confidence: 99%

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Linear plasmids that integrate into mitochondrial DNA in Neurospora

Bertrand¹,

Griffiths²

1989

Genome

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1989. Linear plasmids that integrate into mitochondrial DNA in Neurospora. Genome, 31: 155 -159. In some field isolates of Neurospora from Hawaii and India, senescence is induced by integration of linear DNA plasmids, kulilo and muranhar, respectively, into mitochondrial (mt) DNA. Although the two plasmids show little homology at the DNA level, both have inverted long terminal repeats, and each potentially encodes a DNA polymerase and a RNA polymerase. Both plasmids generate very long inverted repeats of mtDNA at their ends upon integration into mitochondrial chromosomes. Hence, they appear to integrate by a mechanism that involves pairing of both ends of the plasmid with short stretches of homologous nucleotide sequences in mtDNA. This recombinogenic association apparently generates an origin for an unscheduled round of replication of mtDNA. In the process, the resulting two copies of the mitochondrial chromosome are joined to opposite ends of the plasmid. A model for the senescence-associated accumulation of mtDNAs with plasmid insertion sequences is proposed on the basis of common features that characterize senescence in a variety of filamentous fungi.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Linear plasmids that integrate into mitochondrial DNA in Neurospora

Bertrand¹,

Griffiths²

1989

Genome

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“…By far the most common repeats in the mtDNA of N. crassa are a heterogeneous group of cryptic GC-rich, 30-to 80-bp-long palindromic nucleotide sequences, some of which contain two closely spaced PstI restriction sites (65). These sequences are situated almost exclusively in the noncoding segments of mtDNA that are located between genes, and numerous copies are widely distributed throughout the mitochondrial chromosome.…”

Section: Discussionmentioning

confidence: 99%

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

Bertrand¹,

Wu²,

Seidel-Rogol³

1993

Mol. Cell. Biol.

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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 naturaldeath 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 Pstl 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 ofN. 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.In Neurospora crassa, a recessive mutation in the nd (natural-death) locus on linkage group I causes a progressive deterioration of the growth and reproductive potentials of asexually propagated mycelia (57). Phenotypically, the process is manifested as an accelerated senescence syndrome and leads to cell death after two to four sequential (weekly) passages of asexual spores (conidia) to fresh agar slants (56, 57). Consequently, the mutant has been used as a model system for the study of cellular aging (38,44,47,50,52). The most recent of these studies has shown that the nd mutation causes the progressive and coordinate loss of several different mitochondrial functions in growing and stationary-phase mycelia (50, 56). The accelerated degeneration of the respiratory capacity of the cells is paralleled by the appearance of a rather heterogeneous population of grossly altered mitochondrial DNAs (mtDNAs) (56). These observations led to the proposal that the wild-type allele of the nd gene codes for a protein that protects the mitochondrial chromosome from intra-and intermolecular recombination or breakage events that potentially cause deletions, inversions, and other deleterious rearrangements (56).In recent years, other senescence syndromes have been studied extensively in the filamentous fungi, but none of these is caused by mutation of a nuclear gene (reviewed in reference 35). Instead, the predisposition to senesce prematurely and the symptoms that are associated with these aging processes are inherited maternally. Furthermore, it has been shown repeat...

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“…Numerous reports indicate that fungal senescence is associated with age-dependent activity of plasmids of mitochondrial origin (see Esser et al, 1986 ;Nevers et al, 1986 ;Gaubatz, 1990 ;Osiewacz, 1990Osiewacz, , 1995Griffiths, 1992 for extensive reviews on this topic). Most of these senescence-associated plasmids possess characteristics of TEs.…”

Section: Te-associated Aging In Fungimentioning

confidence: 98%