Phenotypic differences between the sexes evolve largely because selection favours a different complement of traits in either sex. Theory suggests that, despite its frequency, sexual dimorphism should be generally constrained from evolving because the sexes share much of their genome. While selection can lead to adaptation in one sex, correlated responses to selection can be maladaptive in the other. In this thesis I use Drosophila to examine the extent to which the shared genome constrains the evolution of sexual dimorphism and whether the sex chromosomes might play a special role in resolving intralocus sexual conflict. Gene expression data shows that intersexual genetic correlations are generally high, suggesting that genes often affect both sexes. The intersexual genetic correlation is negatively associated with sex-bias in expression in D. melanogaster, and the rate of change in sex-bias between D. melanogaster and six closely related species, showing that a sex-specific genetic architecture is a prerequisite for the evolution of sex difference. In further studies I find that genetic variance affecting lifespan is found in the male-limited Y chromosome within a population, which could offer a route to the evolution of further sexual dimorphism in lifespan, though the amount of variance was small suggesting adaptive potential from standing genetic variance is limited. Genetic variance on the X chromosome is also expected to be depleted once the sex chromosomes evolve, but here I find no evidence of depletion in either sex. Dosage compensation does not appear to double the male X-linked genetic variance, but this effect may be complex to detect. Finally, the X chromosome appears to be enriched for sex-specific genetic variance, and the consequences of this are explored using a variety of analytical methods to test biologically meaningful aspects of G-matrix structure. In summary, this thesis suggests that the evolution of sexual dimorphism is generally constrained by the shared genome, but intralocus sexual conflict could be resolved by novel mutations on the Y chromosomes, and by standing sex-specific genetic variance on the X chromosome. It highlights a special role for the X chromosome in the evolution of sexual dimorphism.

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The independent evolution of the sexes may often be constrained if male and female homologous traits share a similar genetic architecture. Thus, cross-sex genetic covariance is assumed to play a key role in the evolution of sexual dimorphism (SD) with consequent impacts on sexual selection, population dynamics and the speciation process. I used quantitative genetics tools to assess the importance of sex-specific genetic variance in facilitating the evolution of body mass and horn size SD in wild bighorn sheep from Ram Mountain, Alberta. I also developed a bighorn sheep genetic linkage map composed of 247 microsatellite markers to gain insights about the genetic architecture of trait variation. Finally, I conducted systematic reviews and meta-analyses of published cross-sex genetic correlations (rMF, a standardized estimate of cross-sex genetic covariance) to test basic hypotheses about the importance of sex-specific genetic variance in the evolution of SD and mechanisms responsible for generating such variance. My results demonstrated that sex-specific genetic variance was present in bighorn sheep and that it likely played an important role in alleviating intralocus sexual conflicts. The quantitative trait locus (QTL) mapping analysis resulted in the identification of numerous loci influencing body mass and horn dimensions, some of which had apparent sex-specific effects. An analysis of 553 rMF estimates recovered from 114 published sources allowed demonstrating that 1) the evolution of SD was generally constrained by positive cross-sex genetic covariance, 2) levels of SD were often sub-optimal, and 3) sex-specific genetic variance was an important mechanism allowing the evolution of SD. In addition, I confirmed the long-standing hypothesis of a general decline in rMF with age. Sexual dimorphism is an important evolutionary phenomenon, but our understanding of its evolution is still limited. After decades of speculation, my research has provided clear empirical evidence for the importance of sex-specific genetic variance in allowing its evolution. / Ecology

Sexual antagonism occurs when there is a difference between the optimal strategy of males and females to achieve maximum fitness. Interactions between sexually antagonistic alleles within a locus (intralocus sexual conflict; IASC) means that a mutation can be beneficial for one sex and deleterious for the other. In a recent genome-wide association study in Drosophila melanogaster, several different candidate genes containing antagonistic single-base polymorphisms were identified. In order to validate the sexual antagonistic effects of one of the candidate genes, Laminin A (LanA; chromosome 3), the wild-type alleles 1 and 2 of LanA were recreated in the Canton-S genetic background using CRISPR/Cas9 gene editing. Previous observations showed that homozygotes with allele 2 died, which resulted in this study where the aim was to investigate why flies of D. melanogaster with two copies of this wild-type was apparently lethal and at what developmental stage they died. Four different lines were available, three with allele 1 and one with allele 2. Virgin females that were heterozygous for the TM6B balancer from the each line were divided into two groups. Half were mated with heterozygous males of the same allele and half with heterozygous males of the opposite allele in tubes prepared with a limited amount of dry yeast. The females were then placed in individual tubes for oviposition. The number of eggs, unhatched eggs, wild-type-/tubby- pupae and adults were then counted as the offspring underwent development. The results showed a higher mortality in the larval stage in the genotype A2/A2, and that no pupae/adults were wild-type A2 homozygotes. There was a significant relationship between genotype and each treatment. Since mortality was higher for genotype A2/A2 in the larval stage and that there were no surviving wild-type pupae, it shows that they do not die immediately after fertilization but at a later larval stage. With the help of the results, this study can confirm the hypothesis that lines of D. melanogaster with all A2 do not lose their balance chromosome, but not why it happened. To be able to answer this question, further studies are required based on other hypotheses and questions. / Sexuell antagonism uppstår när det finns en skillnad mellan hanar och honors optimala strategi för att uppnå maximal fitness. Interaktioner mellan sexuellt antagonistiska alleler inom ett lokus (intralocus sexual conflict; IASC) innebär att en mutation kan vara fördelaktig för ett av könen och skadligt för det andra. I en nyligen utförd studie gjordes en ”genome-wide association study” på Drosophila melanogaster där flera olika kandidatgener innehållande antagonistiska enbaspolymorfier identifierades. I syfte att validera sexuellt antagonistiska effekter på en av kandidatgenerna, Laminin A (LanA; kromosom 3), återskapades vildtyp allelerna 1 och 2 av LanA med Canton-S bakgrund med hjälp av CRISPR/Cas9. Tidigare observationer visade att homozygoter med allel 2 dog, vilket mynnade ut i denna studie där syftet var att undersöka varför flugor av D. melanogaster med två kopior av vildtypen dör och i vilket utvecklingsstadium det sker. Fyra olika linjer var tillgängliga, tre med allel 1 och en med allel 2. Jungfruhonor som var heterozygota för TM6B balanskromosom från vardera linje delades upp i två lika stora grupper. Ena gruppen parades med heterozygota hanar med samma allel och andra gruppen med heterozygota hanar av motsatt allel i rör preparerade med en begränsad mängd torrjäst. Honorna placerades sedan i individuella rör för äggläggning. Antalet ägg, okläckta ägg, vildtyp-/tubby- puppor och vuxna räknades under tiden som avkommorna utvecklades. Resultaten visade på en högre mortalitet i larvstadiet i genotypen A2/A2 och att inga puppor/vuxna var vildtyp A2 homozygoter. Det fanns ett signifikant samband mellan genotyp och varje behandling. Då mortaliteten var högre för genotyp A2/A2 i larvstadiet och att det inte fanns några överlevande vildtyp-puppor visar det att de inte dör direkt efter fertilisering utan i ett senare larvstadie. Studien kan med hjälp av resultatet bekräfta hypotesen om att linjer av D. melanogaster med alla A2 inte förlorar sin balanskromosom men inte varför detta sker. För att kunna svara på den frågan krävs ytterligare studier baserat på andra hypoteser och frågeställningar.

Anisogami och sexuella konflikter kan vara grunden till flera fall av könslig dimorfism. Intralokus sexuell konflikt uppstår när alleler vid ett genetiskt lokus har en antagonistisk effekt på fitness hos hanar och honor. Helgenomstudier har pekat ut flera sexuellt antagonistiska kandidatgener hos Drosophila melanogaster. En av dem, CG15170, har återskapats med hjälp av genediteringstekniken CRISPR/Cas9. Den här genen är intressant då populationer med en viss allel, A1, inte förlorar balanser kromosomen, förmodligen på grund av negativ fitnesspåverkan från den återskapade allelen A1. I den här studien undersöktes om fertiliteten hos honor och ägg-till-vuxen överlevnaden är negativt påverkad. Detta gjordes genom att antalet lagda ägg och proportionen av lagda ägg som utvecklades till vuxna individer hos honor av D. melanogaster homozygota för A1 eller A2 alleler mättes. Resultatet från de statistiska tester som utfördes visade ingen signifikant skillnad mellan honor med A1 och A2 alleler varken för antalet lagda ägg eller proportionen av ägg som utvecklades till vuxna. Däremot upptäcktes en signifikant skillnad mellan de två allelerna i antalet vuxna honor som överlevde parningen i den första delen av försöket. Denna studie kan inte påvisa att fekunditeten hos honorna och den tidiga överlevnadsgraden hos deras avkommor skulle vara olika för honor med A1 respektive A2 alleler. Det bör i stället vara någon annan del av livscykeln som påverkas av att A1 inte förlorar balanser kromosomen men vilken kan ej fastställas utifrån den här studien. / Anisogamy and sexual conflict may be the basis of several cases of sexual dimorphism. Intralocus sexual conflict occurs when alleles at a genetic locus have an antagonistic effect on the fitness of males and females. Genome wide association studies have pointed out several candidate genes for sexual antagonism in Drosophila melanogaster. One of them, CG15170, has been recreated with the gene editing technique CRISPR/Cas9. This gene is interesting because populations with one particular allele, A1, do not lose the balancer chromosome, probably because of negative effects off the allele on fitness. In this study, the fertility and egg-to-adult survival of eggs laid by females was investigated to see if these traits were adversely affected by the recreated allele A1.  This was done by measuring the number of eggs laid by females of D. melanogaster, homozygous for A1 or A2 alleles, and also by measuring the proportion of eggs that developed to adults. The results of the statistical tests that were performed showed no significant difference between females with A1 and A2 alleles, not for the number of eggs laid nor the proportion of eggs that developed into adults. However, a significant difference was detected between the two alleles in the number of adult females that survived the first courtship and mating part of the experiment. Probably some other part of the life cycle is affected by A1 not losing the balancer chromosome, but which cannot be determined by this study.

Sexual conflicts arise when there is a difference in how females and males of a species or population achieve their maximum reproductive fitness. In intralocus sexual conflicts, alleles at a given locus are exposed to conflicting, or antagonistic, selection pressures. Based on a Genome-wide association study on sexually antagonistic genes in Drosophila melanogaster (fruit flies), the aim of this study was to investigate whether the candidate gene CG3598 exhibits sexually antagonistic effects on fitness between the 2 identified alleles of the gene. The study was performed on females from a Canton-S population of D. melanogaster who, by genetic manipulation through CRISPR Cas9, carried one of the 2 alleles of the CG3598. 6 excision lines of females had allele 1 and 5 excision lines had allele 2. The females were mated with "wild type" males from a Canton-S population in mediums prepared with about 6 mg of live dry yeast, after which the females were moved to separate mediums to lay their eggs. After 12 days, the adult offspring were counted and statistical calculations were performed on the average number of offspring per female for each line and allele. An Independent sample t-test showed that the females’ average fecundity did not differ between alleles (p = 0.059) and a Nested ANOVA analysis indicated that the average fecundity for each line within each allele differed (p = 0.023). Due to the fact that similar studies have found the same result, it may be necessary to investigate and possibly change the experimental design of the method to enable competition between females with different genetic conditions in order to observe a difference in fertility based on the females' ability to compete. / Sexuella konflikter uppstår när det finns en skillnad i hur honor och hanar i en art eller population uppnår sin maximala reproduktiva fitness. Vid intralocus sexuella konflikter utsätts alleler vid ett givet locus för motstridiga, eller antagonistiska, selektionstryck. Baserat på en Genome-wide association study om sexuellt antagonistiska gener hos Drosophila melanogaster (bananflugor) syftade denna studie till att undersöka huruvida genkandidaten CG3598 uppvisar sexuellt antagonistiska effekter på fitness mellan de 2 identifierade allelerna av genen. Undersökningen utfördes på honor från en CantonS-population av D. melanogaster som genom genmodifiering av CRISPR Cas9 bar en av de olika alleler av genen CG3598. 6 linjer av honor bar allel 1 och 5 linjer bar allel 2. Honorna parades med ”wild type”-hanar från en CantonS-population i rör preparerade med ca 6 mg levande torrjäst, varpå honorna förflyttades till separata rör för att lägga sina ägg. Efter 12 dagar räknades de vuxna avkommorna och statistiska beräkningar utfördes på det genomsnittliga antalet avkommor per hona för respektive linje och allel. Ett oberoende t-test visade att honornas genomsnittliga fekunditet inte skiljde sig mellan alleler (p=0,059) och en Nested ANOVA-analys indikerade att genomsnittlig fekunditet för varje linje inom respektive allel skiljde sig (p=0,023). Då även liknande studier funnit samma resultat kan det vara nödvändig att studera och eventuellt förändra den experimentella designen av metoden för att möjliggöra konkurrens mellan honor med olika genetiska förutsättningar för att kunna observera en skillnad i fekunditet baserat på honornas förmåga att konkurrera.