Neurospora Mitochondrial Genes and Mutations
| 1) Sequenced fungal mitochondrial genomes |
| 2) Mitochondrial genes and mutants in Neurospora crassa |
Neurospora crassa mtDNA Genbank file
mtDNA Mutations in Neurospora
The genetic analysis of Neurospora mitochondria began in 1952 when Mitchell and Mitchell (1952) isolated the "[poky]" mutant of N. crassa, which became the prototype of mitochondrial mutations in this genus. Poky strains grow slowly for several days, then growth rate gradually accelerates reaching the wild type linear rate after three to four days. Poky strains are deficient for cytochromes aa3 and b (the spectrophotometrically detectable components of complex IV and complex III, respectively), and often have an excess of nuclear-encoded cytochrome c. The cytochrome aa3 and b deficiencies in the [poky] mutant were later found to be associated with a deletion in the promoter for the small rRNA transcript which limits the synthesis of the small ribosomal subunit (see below).
A list of Neurospora mtDNA genes and mutants that are known to affect specific mitochondrial genes or functions is given in the Table. Mitochondrial mutations are commonly pleiotropic and were divided into three groups based on a variety of traits (Bertrand and Pittenger, 1972). Those, like [poky], that have a lag in growth rate, deficiencies in cytochrome aa3 and b, an excess of cytochrome c, and are suppressed by the f nuclear suppressor allele belong to group I. Two mutants, [mi-3] and [exn-5], which show less of a growth lag than [poky], low levels of cytochrome aa3, high cytochrome c, and are suppressed by su([mi-3])-1 comprise group II. Mutants that display an uneven or stop-start growth (“stopper”) phenotype, generally contain low levels of cytochrome aa3 and b, and higher cytochrome c form group III. The [C93] mutant is unusual in that it affects the assembly of the ATP synthase. Thus, it appears to define a new group of extranuclear mutant (Group IV). All the mutants except those in group II show defects of mitochondrial protein synthesis. Those mutants affecting mitochondrial genes for individual components of the electron transport chain are discussed below.
Mutations that occur in the mtDNA are often suppressive. At the experimental level this means that if a mutant/wild type heteroplasmon is established, after subculturing or prolonged growth in a race tube, the culture eventually converts to the mutant phenotype (Pittenger 1956, Garnjobst et al. 1965, Mannella and Lambowitz 1978). An extreme example was the demonstration by Garnjobst et al. (1965) that purified mitochondria from [abn-1] strains injected into a wild type cell resulted in the Abn phenotype after eight subcultures in most recipients.
One possible explanation for the suppressive effect is that a general disturbance in a mitochondrion carrying one or more defective mtDNAs might act as a trigger to promote faster replication of the mitochondrion in order to compensate for energy loss. Two possible disturbances have been suggested, defective oxidative phosphorylation (Bertrand and Griffiths 1989) and defective protein synthesis (Hawse et al. 1990). Effectively, the suppressive phenomenon mimics that demonstrated by certain yeast petite mutants, though the mechanisms by which the mutant mtDNA molecules “takeover” are undoubtedly quite different in the two organisms (MacAlpine et al. 2001).
Several stopper mutants from group III have been shown to contain large deletions or insertions in the mtDNA (Bertrand et al. 1980; de Vries et al. 1986; Gross et al. 1984; Mishra 1991). It has been suggested that the stop-start growth phenotype might be the result of competition between defective DNAs which predominate and less defective and less abundant mtDNAs which must be maintained at some level to allow growth (Bertrand et al. 1980).
