[1][2] Mutagens that create Petites are implicated in increased rates of degenerative diseases and in the aging process.
[3] Over 50 years ago, in a lab in France, Ephrussi, et al. discovered a non-Mendelian inherited factor that is essential to respiration in the yeast, Saccharomyces cerevisiae.
[4] It has been suggested that there is a link between mitochondrial DNA loss and replicative life span (RLS), or the number of times a cell can reproduce before it dies, as it has been found that an increase in RLS is established with the same changes in the genome that enhance the propagation of cells that do not contain mitochondrial DNA.
[4] The petite is characterized by a deficiency in cytochromes (a, a3 + b) and a lack of respiratory enzymes which engage in respiration in mitochondria.
[7] Due to the error in the respiratory chain pathway, 'petite' yeast is incapable of growing on media containing only non-fermentable carbon sources (such as glycerol or ethanol) and forming small colonies when grown in the presence of fermentable carbon sources (such as glucose).
Petite mutants can be generated in the laboratory by using high-efficiency treatments such as acriflavine, ethidium bromide, and other intercalating agents.
[3] Though S. cerevisiae has been extensively studied in this and other areas, it is difficult to say if the molecular mechanisms of this process in the mitochondrial DNA are conserved across other yeast species.
Other yeast species, such as Kluyveromyces lactis, Saccharomyces castellii, and Candida albicans have all shown to produce petite negative mutants.