CMS
Frank SA 1989 The evolutionary dynamics of cytoplasmic male sterility. Am Nat 133:345-376.
- Lewis (1941) ... noticed that if male-sterile individuals have a higher fitness through ovules than do hermaphrodites, a cytoplasmic gene causing male sterility will spread in the population
- data on ovule fitness in male steriles relative to hermaphrodites ranges from rare cases in which male steriles and hermaphrodites have nearly equal ovule fitness (Vaarema and Jääskeläinen 1967) to cases in which the seed output per male-sterile flower is more than twice that per hermaphrodite flower
- Lewis (1941) pointed out that a male-sterile cytoplasmic gene associated with increased ovule fitness continues to spread until checked by some opposing force
- a number of later theoretical studies have analyzed a subset of autosomal-cytoplasmic interactions, population subdivision, pollen limitation, frequency of selfing, inbreeding depression, and pleiotropic fitness effects of both cytoplasmic male-sterile genes and autosomal restorer genes
- Lloyd (1974) ... derived the equilibrium frequency of females as a function of pollinator limitation and relative seed fecundity and viability of hermaphrodites and females
- three studies have assumed that
- (1) autosomal restorer genes and cytoplasmic male-sterility genes are present
- (2) self-fertilized and outcrossed ovules are of equal viability
- (3) the ovule production is the same for both male-sterile and hermaphroditic plants
- these three studies all concluded that male sterility cannot be maintained
- Lloyd (1975, 1976) extended his earlier model ... by also considering selfing and inbreeding depression
- D. Charlesworth and Ganders (1979) extended the models ... by allowing the viabilities of self-fertilized and outcrossed ovules to differ and by assuming that male-sterile plants may have an increased ovule output
- under these assumptions either the population approaches fixation for male sterility or the autosomal restorer gene becomes fixed
- D. Charlesworth (1981) and Delannay et al. (1981) extended the model by showing that polymorphism can be maintained when the cytoplasmic male-sterility or autosomal restorer genes have additional (pleiotropic) effects on ovule fertility or viability
- selection of cytoplasmic variants with any ovule-fertility or viability advantage tends to favor an increase in the frequency of male-sterile individuals
- selection of autosomal variants tends to favor the elimination of male steriles
- the direction of selection differs between the autosomal and cytoplasmic points of view
- there is a conflict of interest
- the conflict is inherent
- it is never discussed explicitly
