Amplification of Nicotiana sylvestris mitochondrial subgenomes is under nuclear control and is associated with phenotypic changes

• Published in: Genetica Vol. 117; no. 1; pp. 17 - 25
• Main Authors: Albert, Béatrice, Lelandais, Christine, Pla, Magali, Leuret, Corine, Vitart, Véronique, Mathieu, Chantal, Sihachakr, Darasinh, Godelle, Bernard, De Paepe, Rosine
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 01.01.2003
• Subjects: Cell Nucleus; DNA, Mitochondrial - genetics; DNA, Plant - genetics; Evolution, Molecular; Gene Amplification - genetics; Genetics; Male sterility; Mitochondrial DNA; Mutation; Nicotiana - genetics; Phenotype; Recombination, Genetic; Restriction Mapping
• ISSN: 0016-6707; 1573-6857
• DOI: 10.1023/A:1022356330794

We have previously shown the presence in a Nicotiana sylvestris protoplast-derived plant of both a nuclear mutation conferring male sterility (ms4) and a mtDNA reorganisation, named U, characterised by the amplification of substoichiometric mtDNA fragments generated by recombination in the parent T mtDNA. Here we show by physical mapping that the recombining repeats are in direct orientation, thus generating two subgenomes both of which are amplified in the U organisation to the detriment of the parent molecule, and are maintained through sexual reproduction. The nuclear ms4 mutation is likely to have play a role in the shift in mitochondrial molecule equilibrium, as higher levels of recombinant fragments were present in protoplast-derived T calli carrying the ms4 allele than in wild type calli or leaves. The MS4 gene could then lead to conflictual situation. However, subgenomic molecules were counter-selected during the regeneration process, suggesting the existence of different selective pressures in differentiated and non-differentiated cells. The U organisation is associated with higher stem height and late flowering, characters that may not be neutral from a selection point of view. The U equilibrium is an unusual example of sudden mtDNA reorganisation, without obvious differences in genetic information and with only a limited phenotypic impact.