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Hitchcock, T. J.

Publications and source records attributed to Hitchcock, T. J..

4 recordsLinked to original sources

Paternal genome elimination, monogenic reproduction, and the evolutionary genetics of atypical sex chromosome systems

Sex chromosomes differ from autosomes in both their ploidy and transmission genetics. Consequently, selection, mutation, and drift may act differently upon them, driving distinct patterns in genetic divergence, diversity, and gene content. Recently, researchers have begun to consider a wider set of organisms with non-standard inheritance and sex-determination systems, however in many cases we lack theory which extends to such cases. One such example is paternal genome elimination (PGE), an unusual reproductive system which has independently evolved in two fly families, the fungus gnats (Sciaridae) and gall midges (Cecidomyiidae), and one order of springtails (Symphypleona). Under PGE, males receive but do not transmit a paternal genome, such that the autosomes and X chromosomes exhibit the same transmission genetics, but with different somatic ploidy. This makes them uniquely suited to test hypotheses about the role of haploid selection in males. Additionally, repeatedly throughout these groups a novel sex determination system - monogeny - has evolved, whereby females produce broods of exclusively one sex. The genetic basis of monogeny partitions the X chromosome into three segments, all displaying distinct inheritance patterns. Here we develop a series of theoretical models adapted to the genetics of these groups, generating testable predictions as to the relative genetic diversity within populations, and divergence between populations. Our results suggest that these species are excellent systems with which to test many fundamental principles in evolutionary genetics.

evolutionary biology↗

Chimerism and altruism

Chimerism spans the tree of life, from mammals and corals to plants and fungi. In such organisms, individuals contain within them cells and genomes from another once distinct member of the population. This chimeric genetic composition may subsequently alter patterns of relatedness not only between those individuals, but also within them. Consequently, we may expect unique patterns of social behaviour in such species. To explore the social evolutionary consequences of chimerism, here we develop a kin-selection model of a structured population. First, we show how somatic and germline chimerism influence patterns of relatedness and play an important role in modulating social behaviour. Specifically, we find that increased heterogeneity of the soma relative to the germline boosts the opportunity for altruism between individuals. We then explore how differences in chimerism levels within the body may generate within-organism differences in the valuation of social partners and thus foment internal conflicts between tissues and organs. Finally, we show how differences in the development of male and female germlines in chimeras provides a novel source of relatedness asymmetry between maternal-origin and paternal-origin genes. Overall, we find that chimerism introduces additional opportunities for internal conflicts over the development of behavioural phenotypes, most of which have been unexplored by empiricists.

evolutionary biology↗

Sexual antagonism in sequential hermaphrodites

Females and males may have distinct phenotypic optima, but share essentially the same complement of genes, potentially leading to trade-offs between attaining high fitness through female versus male reproductive success. Such sexual antagonism may be particularly acute in hermaphrodites, whereby both reproductive strategies are housed within a single individual. Whilst previous models have focused on simultaneous hermaphroditism, we lack theory for how sexual antagonism may play out under sequential hermaphroditism, which have the additional complexities of age-structure. Here we develop a formal theory of sexual antagonism in sequential hermaphrodites. First, we develop a general theoretical overview of the problem, then consider different types of sexually antagonistic and life-history trade-offs, under different modes of genetic inheritance (autosomal or cytoplasmic), and different forms of sequential hermaphroditism (protogynous, protoandrous or bi-directional). Finally, we provide a concrete illustration of these general patterns by developing a two-stage two-sex model, which yields conditions for both invasion of sexually antagonistic alleles and maintenance of sexually antagonistic polymorphisms.

evolutionary biology↗

Sexual antagonism in haplodiploids

Females and males may face different selection pressures, such that alleles conferring a benefit in one sex may be deleterious in the other. Such sexual antagonism has received a great deal of theoretical and empirical attention, almost all of which has focused on diploids. However, a sizeable minority of animals display an alternative haplodiploid mode of inheritance, encompassing both arrhenotoky, whereby males develop from unfertilized eggs, and paternal genome elimination (PGE), whereby males receive but do not transmit a paternal genome. Alongside unusual genetics, haplodiploids often exhibit social ecologies that modulate the relative value of females and males. Here we develop a series of evolutionary-genetic models of sexual antagonism for haplodiploids, incorporating details of their molecular biology and social ecology. We find that: 1) PGE promotes female-beneficial alleles more than arrhenotoky, and to an extent determined by the timing of elimination - and degree of silencing of - the paternal genome; 2) sib-mating relatively promotes female-beneficial alleles, as do other forms of inbreeding, including limited male-dispersal, oedipal-mating, and the pseudo-hermaphroditism of Icerya purchasi; 3) resource competition between related females relatively inhibits female-beneficial alleles; and 4) sexual antagonism foments conflicts between parents and offspring, endosymbionts and hosts, and maternal-origin and paternal-origin genes.

evolutionary biology↗