Abstract
Mitochondrial mutations for resistance to various antibiotics (erythromycin, chloramphenicol, spiramycin, mikamycin) have been obtained in Paramecium aurelia and their properties are reviewed. Using these mitochondrial markers, the interactions between nucleus and mitochondria have been studied in two ways: by microinjection of mitochondria from one stock or species into other stocks and species of P. aurelia and by a genetic study of a nuclear mutation affecting mitochondrial multiplication. Both types of experiments show: (1) that there may exist incompatibility between a given type of mitochondria and the cell into which they are introduced and (2) that through multiplication in the host cell, mitochondrial properties can be modified. The possible basis for incompatibility and host-induced modifications is discussed.