Résumé
Cytoplasmic male sterility (CMS) originates from a mito-nuclear conflict where mitochondrial genes induce male sterility and nuclear genes restore male fertility in hermaphrodites. The first observation of CMS in animals was reported recently in the freshwater snail Physa acuta where it is associated with two extremes divergent mitotypes D and K. The D individuals are male-steriles while male fertility is restored by nuclear genes in K and are found mixed with the most common male-fertile N mitotype in natural populations (i.e. gynodioecy). We compared male and female fitness, growth rate and metabolism between the three mitotypes at two temperatures as this factor influences CMS in gynodioecious plants via alteration of mitochondrial functioning. Temperature did not affect male sterility which depended only on the mitotype and the presence of restorers. Our results provided evidence that CMS is beneficial to female fitness in the absence of restorers while it is costly in their presence, and furthermore driven by body mass, fulfilling a key theoretical condition for the long-term maintenance of gynodioecy. Fitness benefits and costs mediated by differences in body mass are enhanced at cold temperature, suggesting that the system dynamics may vary according to thermal conditions in nature.