The inheritance and population genetics of sex ratio in the butterfly Acraea encedon

In West and East Africa the butterfly, Acraea encedon , occurs in well-defined populations that are often predominantly female. Breeding the butterfly in the laboratory revealed the presence of an all-female strain, which is inherited directly through the female parent. It is probable that the inheritance is controlled by a Y-linked gene, causing meiotic drive in the Y chromosome, but the possibility of cytoplasmic inheritance has not been ruled out. A simple model for the population genetics of a predominantly female population indicates that such a population should rapidly become extinct due to the spreading of the all-female strain, but in most field populations studied extinction does not occur as quickly as predicted, if at all. Three factors which could enable populations to avoid extinction are investigated: suppressing systems, frequency-dependent mating preference and the sequence of emergence of the sexes in normal broods. No positive evidence has yet been found for the existence of a gene or genes capable of suppressing the sex ratio aberration, and no frequency-dependent mating preference was found, but an argument is presented which shows that the sequence of emergence in normal broods could be partly responsible for the maintenance of stable equilibria in predominantly female populations. Attempts to upset the sex ratio in the normal strain by making crosses between widely separated populations were not successful.     

Mitochondrial DNA polymorphism, sex ratio distorters and population genetics in the isopod Armadillidium vulgare.

Two maternally inherited sex ratio distorters (SRD) impose female-biased sex ratios on the wood louse Armadillidium vulgare by feminizing putative males. These SRD are (i) an intracytoplasmic bacterium of the genus Wolbachia, and (ii) another non-Mendelian element of unknown nature: the f element. Mitochondrial DNA variation was investigated in A. vulgare field populations to trace the evolution of host-SRD relationships and to investigate the effect of SRD on host cytoplasmic polymorphism. The Wolbachia endosymbionts showed no polymorphism in their ITS2 sequence and were associated with two closely related mitochondrial types. This situation probably reflects a single infection event followed by a slight differentiation of mitochondria. There was no association between the f element and a given mitochondrial type, which may confirm the fact that this element can be partially paternally transmitted. The spreading of a maternally inherited SRD in a population should reduce the mitochondrial diversity by a hitchhiking process. In A. vulgare, however, a within-population mtDNA polymorphism was often found, because of the deficient spread of Wolbachia and the partial paternal inheritance of the f element. The analysis of molecular variance indicated that A. vulgare populations are genetically structured, but without isolation by distance.     

The genetics of phenotypic plasticity I. Heritability

Methods for estimating the genetic component of phenotypic plasticity are presented. In the general case of clonal replicates or full-sibs raised in several environments, the heritability of plasticity can be measured as the ratio of the genotype-environment interaction variance to the total phenotypic variance. In the special case of only two environments plasticity also can be measured as the difference among environments in genotype or family means. In that case, the heritability of plasticity can be measured as either a ratio of variance components or as the slope of a parent-offspring regression. The general measure suffers because no least-square standard errors have been developed, although they can be calculated by maximum-likelihood or bootstrapping techniques. For the other two methods least-square standard errors can be calculated but require very large experiments for statistical significance to be achieved. The heritability measures are compared using data on plasticity of thorax size in response to temperature in Drosophila melanogaster. The heritability estimates are all in close agreement. Models of the evolution of phenotypic plasticity have treated it as a trait in its own right and as a cross-environment genetic correlation. Although the first approach is the one used here, neither one is preferred.     

The primary sex ratio under environmental sex determination

The ESS primary sex ratio (male/female) under environmental sex determination (ESD) is shown to be equal to the ratio of the average fertility of a female to the average fertility of a male. Thus, depending upon how male and female fertility change over the environmental variable causing ESD, the primary sex ratio may be either male or female biased, or neither. The primary sex ratio thus contains information as to how male and female fertilities change with the environment.     

The sex ratio in anencephaly

It is shown that the well known excess of females in anencephalic births is statistically significant when compared with (a) the general population and (b) their normal sibs.There is also a statistically significant difference between the sex ratio of anencephalic births and that of spina bifida births which suggests that there is a definite difference in the genetic component of their aetiology.These results are discussed with reference to the genetics of anencephaly and spina bifida and a genetic model of the inheritance of the genetic component of anencephaly is given. The significance of a possible cytoplasmic factor is also considered.     

The sex ratio of Japanese twins

I have previously suggested that the sex ratios of multiple births registered in Japan are biased. Data published by Imaizumi[1982a, b] are consistent with the suggestion that this alleged bias diminished during the two decades preceding 1974. If true, this would provide additional evidence for my claim that the sex ratio of monozygotic twins is low.     

The question of adaptive sex ratio in outcrossed vertebrates.

Of various published theories of adaptive control of progeny sex ratio only two are plausible, a physiological theory by Trivers & Willard, and a demographic theory by Verner. The first applies to species in which sons and daughters impose different costs on parents, and in which only one or very few young are produced at once. They ought to show positive correlations in the sex of successive offspring and high sex-ratio variance among progenies. Verner's theory postulates a minimization of competition for mates in neighbourhoods subject to random fluctuation in sex ratio. Optimal progenies would exactly match the population's evolutionary equilibrium sex ratio. There would be little variance among progenies. Evidence from vertebrates is unfavourable to either theory and supports, instead, a non-adaptive model, the purely random (Mendelian) determination of sex. The apparent absence of parental control of progeny sex ratio is a serious theoretical difficulty.     

The economics of clinical genetics services. I. Preview.

To an ever increasing extent, a variety of economic factors are affecting the delivery of clinical genetics services. These economic factors, which we enumerate with an historical perspective, influence how genetics professionals, patients, and third-party payers relate to genetics services. From the perspectives of each of these interested parties, the deficiency of objective information about the current economic situation is striking. The recent history of charges and reimbursement for our genetics clinic illustrates both one kind of data that is readily available and how modification of administrative procedures can improve the economic balance sheet. However, several characteristics of clinical genetics limit the possibility of economic self-sufficiency.     

Evolution of sex I. Primitive sex

Sex is a process of fusion of separate hereditary determinants. The advantages which could accrue from such fusions are protection against deleterious mutations and the possibility of combining favorable alleles into a single individual. If the fitness of the aggregate resulting from fusion is greater than its parts there will be strong selective pressure to perpetuate the aggregate in all progeny. Continued fusion presents problems though and new environmental conditions may occur which favor segregation. Segregation is also favored because of the existence of favorable recessive mutations. It is argued that the balance between these alternative goals of phenotype stability versus variety achieved an effective compromise with the development of the meiosis-fusion-mitosis cycle.     

The genetics of sex ratio distortion by cytoplasmic infection under maternal and contagious transmission: An epidemiological study

Nuclear and cytoplasmic determinants jointly influence the sex ratio in several organisms. A mathematical model of a maternally inherited extra-chromosomal agent that affects the fitness of its carriers and distorts the sex ratio in their broods is analyzed. The agent is transmitted through the cytoplasm from mother to daughter, or it may pass contagiously among females of the same generation. It is shown that under natural selection the deviation between the population sex ratio and Fisher's optimum value evolves to a minimum.