Rescue of a maize mitochondrial cytochrome oxidase mutant by tissue culture^†

Abstract

SummaryThe maize NCS6 mitochondrial mutation is a partial deletion of the cytochrome oxidase subunit 2 gene (cox2) that survives heteroplasmically in the plant. Mutant mitochondria segregate from normal mitochondria during somatic development giving rise to defective sectors on the plants, including areas of kernel abortion on the ears. Embryos from NCS6 kernels can be rescued by tissue culture. Slowly growing Type II callus derived from one of these embryos has been shown by PCR analysis to be homoplasmic for the mutation, carrying only the defective mitochondrial cox2 gene. Most of the rescued embryos were heteroplasmic for normal and mutant genes and heteroplasmy was maintained in the callus cultures. However, when suspension cultures were initiated from heteroplasmic calli, normal cells were shown to have a selective advantage. When the homoplasmic cox2 mutant callus cultures were placed on regeneration medium, planUets did not regenerate. Heteroplasmic calli were capable of regeneration under the same conditions. These studies suggest that the functioning of mitochondrial cytochrome oxidase is not essential for growth as callus, but is required for the differentiation and development of plants.

Decreasing Electron Flux through the Cytochrome and/or Alternative Respiratory Pathways Triggers Common and Distinct Cellular Responses Dependent on Growth Conditions

“…This is largely because of the fact that, with the exception of complex I inactivation, total inactivation of the cytochrome pathway is lethal, and plants lacking cytochrome c, which transfers electrons from complex III to IV, or plants deficient in complex IV are not viable (Gu et al, 1994;Welchen et al, 2012). Thus, although a variety of studies have analyzed the effects of the abolition of complex I activity (Dutilleul et al, 2003a(Dutilleul et al, , 2003bNoctor et al, 2004;Meyer et al, 2009;Braun et al, 2014), AOX (Fiorani et al, 2005;Giraud et al, 2008), or alternative NAD(P)H dehydrogenase activities (Wallström et al, 2014a(Wallström et al, , 2014b, to date, there are a limited number of studies on plants with severely limited electron transport through the cytochrome chain.…”

“…Lethality of a complete abolition of complex IV activity has been suggested by the characterization of the nonchromosomal stripe mutants in Zea mays (Gu et al, 1994). However, plants with greatly reduced amounts of respiratory chain complexes can be obtained through so-called surrogate mutants.…”

Suppression of Repeat-Mediated Gross Mitochondrial Genome Rearrangements by RecA in the Moss Physcomitrella patens

“…The subgenome exists in some proportion relative to the normal genome, a condition known as heteroplasmy, and when the amount of the normal genome falls below a threshold level required for normal function of mitochondria, a mutant phenotype is seen. The effect of mtDNA heteroplasmy is discussed in a number of studies in maize (Zea mays; Gu et al, 1993Gu et al, , 1994Marienfeld and Newton, 1994). The phenotypes of the RECA1 disruptant, including the defect in plant growth and development as well as mitochondrial abnormalities, may be caused by the effect of mtDNA heteroplasmy involving the subgenomes with the truncated gene, which were derived from the induced aberrant recombination.…”

Phage-Type RNA Polymerase RPOTmp Performs Gene-Specific Transcription in Mitochondria of Arabidopsis thaliana

“…Complex I function is not essential in Arabidopsis, but its absence leads to developmental defects (Falcon de Longevialle et al, 2007). Complex IV, on the other hand, is vital for plant development (Gu et al, 1994). The importance of RPOTmp for the expression of principal mitochondrial components adds substantially to present views of the contribution of transcriptional processes to steady state RNA pools and protein synthesis in plant mitochondria.…”