Fluctuating asymmetry (FA) is small deviations from perfect symmetry in normally bilaterally symmetrical traits. We examined the relationship between FA of five body traits (ear height, length of three digits, and ankle circumference) and self-reported scores of physical and verbal aggression in a sample of 90 boys aged 10 to 15 years. The relationships between FA and scores of aggression (particularly physical aggression) were found to be negative; in other words, the most symmetrical boys showed highest aggression. One trait (ankle (...) circumference) showed the characteristics of “ideal” FA—parametric mean of zero and a normal distribution. Mean asymmetries calculated from six repeated measures of ankle FA in 30 subjects taken over a period of five months showed strong negative associations with scores of physical aggression which were independent of age, height, and weight.It is argued that soft tissue “cyclical” FA (as opposed to “fixed” bony FA) is dependent on the secretion of hormones: for example, cortisol. Causal associations between behavioral traits such as aggresion and hormones will lead to similar correlations between FA and behavior. (shrink)

Under the influence of recurrent deleterious mutation and selection, asexual and sexual populations reach a deterministic equilibrium with individuals carrying 0,1,2,. . . harmful mutations. When a favourable mutation (aA) occurs in an asexual population it will usually occur in an individual who has one or more (k) deleterious mutations. Muller's ratchet then applies as A will thereafter never occur in an individual with less than k mutations. If the selective advantage of A is less than the selective disadvantage of (...) k harmful mutations then A will not spread. If it is greater it may spread carrying k deleterious mutations to fixation. Sexual populations are not affected in this way. A will spread through the population experiencing genomes with 0,1,2,. . . deleterious mutations in accordance with the deterministic equilibrium. (shrink)

Under the influence of deleterious mutation and selection a population will reach equilibrium and contain individuals with [0, 1, 2 - - mutations.] This deterministic equilibrium distribution is exactly the same for asexual and sexual populations. The size of the optimal class , i.e. the class with the smallest number of mutations, is determined by the genome mutation rate and the average selective disadvantage of the mutations. A large U and small s gives a very small n o. If n (...) o is small in an asexual population it will be lost by drift and this causes a reduction in the mean fitness of the population . It is argued that diploidy increases U and reduces s. Values of U and s observed from Drosophila indicate a diploid would have a vanishingly small n o. The argument suggests Muller's ratchet is more powerful than previously accepted in asexual species derived from diploid sexual ancestors. (shrink)

There is evidence that asexual reproduction has a long-term disadvantage when compared to sexual reproduction. This disadvantage is usually assumed to arise from the more efficient incorporation of advantageous mutations by sexual populations. We consider here the effect on asexual and sexual populations of changes in the fitness of harmful mutations. It is shown that the re-establishment of equilibrium following environmental change is generally faster in sexual populations, and that the mutational load experienced by the sexual population can be significantly (...) less during this period than that experienced by an asexual one. Changes in the fitness of harmful mutations may therefore impose a greater long-term disadvantage on asexual populations than those which are sexual. (shrink)

A model is proposed which implicates molecular recognition systems as the major controlling factors in life cycle expression. It is envisaged that such systems are important in immune functioning and catabolic, metabolic molecule recognition at both inter- and intea-cellular level. These recognition systems have the following characteristics: Specific recognition molecules , e.g. vertebrate antibodies, invertebrate agglutinins and plant agglutinins may recognise specific substances, e.g. antigens, catabolic and metabolic molecules. The range of possible recognisable substances is very wide and variable. The (...) recognisers may themselves be recognised by other recognisers. Recognisers are usually produced in large amounts only on presentation of the appropriate recognisable molecule. The progressive introduction of new recognisable molecules increases the recogniser interaction, this interaction causing depression of some recogniser types and facilitation of other types among which may be recognisers specific for self components . Low juvenile viability is associated with a restricted range of available recognisers, high adult viability with increasing recogniser range and some auto-immunity/immune depression, senescence with a wide range of available recognisers and extensive auto-immunity/immune depression.Life cycle patterns and their control are discussed. It is suggested control mechanisms may include: Dietary restriction and in some periods complete nutritional abstinence. Specific recogniser depression, genes implicated here are the various antigens found on cell surfaces, in the serum and in various body fluids of vertebrates, e.g. ABO, MNSs, P, Rh, Le and other blood groups, the ABO and Le secretor antigens and the HL-A antigens. In addition the immune response and mixed lymphocyte culture loci are implicated. Finally life cycle control is discussed with relation to sexual selection. (shrink)