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. 1989 Oct;9(10):4259–4264. doi: 10.1128/mcb.9.10.4259

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

B L Seidel-Rogol 1, J King 1, H Bertrand 1
PMCID: PMC362505  PMID: 2531276

Abstract

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.

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Selected References

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