Mutagen sensitivities and mutator effects of MMS-sensitive mutants in neurospora

Käfer, Etta

doi:10.1016/0027-5107(81)90176-7

Cited by 32 publications

(17 citation statements)

References 51 publications

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“…The MMS-sensitivity was determined in two different ways: First, the wild type and mutant conidia were treated with 0 5 % of MMS for different time intervals and were then plated on normal growth medium to examine their capabilities in repairing the damages inflicted on DNA, as estimated by their survival frequency. Such a lack of the dose response has been reported earlier (Kafer, 1981). These data are depicted in Figs 3 and 4.…”

Section: Resultssupporting

confidence: 83%

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Biochemical genetics of Neurospora nuclease II: Mutagen sensitivity and other characteristics of the nuclease mutants

Mishra

Forsthoefel

1983

Genet. Res.

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Five new nuc mutants of Neurospora crassa iyere characterized for their relative sensitivities to different mutagens (UV, MNG, MMS), to mitomycin-C and to histidine; latter has been shown to inhibit the growth of certain UV sensitive mutants. These mutants were also compared for their capabilities for spontaneous mutation as determined by resistance to p-fluoro-phenylalanine. Based on these characterization, the mutants seem to belong to two groups. The first group included nuc-3 and nuc-6 which showed sensitivity to all mutagen tested and possessed capability for a very high frequency of spontaneous mutation (i.e. mutator effect). The second group included nuc-4, nuc-5 and nuc-7; these were as resistant to different mutagens as the wild type strain, but possessed an antimutator effect (i.e. the frequency of spontaneous mutation by these three mutants were at least 05-100 x less than the wild type strains). There was some variation in these properties of mutants belonging to the two groups. Among all the five nuc mutants, nuc-3 was characterized by extreme sensitivity to all mutagens. None of the five nuc mutants were sensitive to histidine. The properties of nuc mutants are discussed in relation to their possible role in DNA repair and recombination.

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Section: Resultssupporting

confidence: 83%

“…A number of genes are known to control mutagen sensitivities in Neurospora crassa (Schroeder, 1975;Kafer, 1981;Fraser & Kafer, 1979;Delange & Mishra 1981, 1982. The present nuc mutants do not appear to be allelic to either of the previously described mutants because of their particular location on the linkage group II (right to the arg-12).…”

Section: Discussionmentioning

confidence: 62%

Biochemical genetics of Neurospora nuclease II: Mutagen sensitivity and other characteristics of the nuclease mutants

Mishra

Forsthoefel

1983

Genet. Res.

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“…The deduced amino acid sequence showed that the mus-11 gene encodes the homolog of S. cerevisiae Rad52p (paper in preparation). The mus-11 mutant showed a low level of induced mutability and a high frequency of spontaneous mutation (Kafer 1981). These results indicate that the mutagenesis process diers in in each of the mei-3, mus-25 and mus-11 mutants, although it is presumed that these gene products work as a complex, at the same repair stage, as they do in S. cerevisiae.…”

Section: Discussionmentioning

confidence: 94%

Characterization of the Neurospora crassa mus-25 mutant: the gene encodes a protein which is homologous to the Saccharomyces cerevisiae Rad54 protein

et al. 2000

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Characterization of the Neurospora crassa mus-25 mutant suggests that it is defective in recombination repair and belongs to the uvs-6 epistasis group. It shows a high sensitivity to the alkylating agents methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but not to UV radiation. It is barren (i.e. does not produce ascospores) in homozygous crosses. The frequency of MMS-induced mutations at the ad-3 loci is approximately three times higher than in the wild type. The ratio of homologous to nonhomologous integration of the pMTR::HYG plasmid is much lower than in wild type. The mus-25 mutant is epistatic to the mei-3 mutant for MMS sensitivity. mei-3, which is a homololog of the Saccharomyces cerevisiae gene RAD51, is a member of the uvs-6 epistasis group which contains several genes that are homologous to recombination repair genes in other organisms. The mus-25 gene was cloned by identifying a genomic DNA fragment which complements the MMS sensitivity of the mutant. The amino acid sequence deduced from the cloned DNA showed a high degree of homology to the Rad54 protein, which is involved in recombinational repair in S. cerevisiae. Comparison of the nucleotide sequences of the genomic and cDNAs of the mus-25 gene revealed an ORF of 2505 bp with a single 118-bp intron beginning immediately after the second nucleotide of the AUG start codon. The molecular weight of the deduced gene product was 93.5 kDa. The transcript level was raised within 60 min after UV irradiation or MMS treatment, as also observed for the expression of the other N. crassa recombinational repair genes, suggesting the existence of a common mechanism which induces expression of the recombinational repair genes in response to DNA damage.

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“…However, mus-10 did not display several phenotypes common to other members of the uvs-6 epistasis group: chromosomal instability, a high sensitivity to histidine, and the inability to produce viable ascospores in homozygous crosses Kafer and Perlmutter 1980;Kafer 1981;Schroeder 1986;Watanabe et al 1997;Handa et al 2000;Sakuraba et al 2000). Furthermore, the frequencies of spontaneous and radiation-induced mutation observed in mus-10 were similar to those of a wild-type strain (Kafer 1981). Past efforts to uncover the nature of these discrepancies or the function of the mus-10 gene product have been uninformative.…”

mentioning

confidence: 92%

Deletion of a Novel F-Box Protein, MUS-10, in Neurospora crassa Leads to Altered Mitochondrial Morphology, Instability of mtDNA and Senescence

Kurashima¹,

Chae²,

Sawada³

et al. 2010

Genetics

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While mitochondria are renowned for their role in energy production, they also perform several other integral functions within the cell. Thus, it is not surprising that mitochondrial dysfunction can negatively impact cell viability. Although mitochondria have received an increasing amount of attention in recent years, there is still relatively little information about how proper maintenance of mitochondria and its genomes is achieved. The Neurospora crassa mus-10 mutant was first identified through its increased sensitivity to methyl methanesulfonate (MMS) and was thus believed to be defective in some aspect of DNA repair. Here, we report that mus-10 harbors fragmented mitochondria and that it accumulates deletions in its mitochondrial DNA (mtDNA), suggesting that the mus-10 gene product is involved in mitochondrial maintenance. Interestingly, mus-10 begins to senesce shortly after deletions are visualized in its mtDNA. To uncover the function of MUS-

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Mutagen sensitivities and mutator effects of MMS-sensitive mutants in neurospora

Cited by 32 publications

References 51 publications

Biochemical genetics of Neurospora nuclease II: Mutagen sensitivity and other characteristics of the nuclease mutants

Biochemical genetics of Neurospora nuclease II: Mutagen sensitivity and other characteristics of the nuclease mutants

Characterization of the Neurospora crassa mus-25 mutant: the gene encodes a protein which is homologous to the Saccharomyces cerevisiae Rad54 protein

Deletion of a Novel F-Box Protein, MUS-10, in Neurospora crassa Leads to Altered Mitochondrial Morphology, Instability of mtDNA and Senescence

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