liu.seSearch for publications in DiVA
Change search
Link to record
Permanent link

Direct link
BETA
Publications (10 of 12) Show all publications
Zajitschek, F., Zajitschek, S. R. K., Canton, C., Georgolopoulos, G., Friberg, U. & Maklakov, A. A. (2016). Evolution under dietary restriction increases male reproductive performance without survival cost. Proceedings of the Royal Society of London. Biological Sciences, 283(1825), 20152726
Open this publication in new window or tab >>Evolution under dietary restriction increases male reproductive performance without survival cost
Show others...
2016 (English)In: Proceedings of the Royal Society of London. Biological Sciences, ISSN 0962-8452, E-ISSN 1471-2954, Vol. 283, no 1825, p. 20152726-Article in journal (Refereed) Published
Abstract [en]

Dietary restriction (DR), a reduction in nutrient intake without malnutrition, is the most reproducible way to extend lifespan in a wide range of organisms across the tree of life, yet the evolutionary underpinnings of the DR effect on lifespan are still widely debated. The leading theory suggests that this effect is adaptive and results from reallocation of resources from reproduction to somatic maintenance, in order to survive periods of famine in nature. However, such response would cease to be adaptive when DR is chronic and animals are selected to allocate more resources to reproduction. Nevertheless, chronic DR can also increase the strength of selection resulting in the evolution of more robust genotypes. We evolved Drosophila melanogaster fruit flies on DR, standard and high adult diets in replicate populations with overlapping generations. After approximately 25 generations of experimental evolution, male DR flies had higher fitness than males from standard and high populations. Strikingly, this increase in reproductive success did not come at a cost to survival. Our results suggest that sustained DR selects for more robust male genotypes that are overall better in converting resources into energy, which they allocate mostly to reproduction.

Place, publisher, year, edition, pages
ROYAL SOC, 2016
Keywords
Drosophila melanogaster; nutrition; dietary stress; adaptation
National Category
Biological Sciences
Identifiers
urn:nbn:se:liu:diva-127788 (URN)10.1098/rspb.2015.2726 (DOI)000374207800007 ()26911958 (PubMedID)
Note

Funding Agencies|Wenner-Gren postdoctoral fellowship; Swedish Research Council; ERC Starting Grant AGINGSEXDIFF

Available from: 2016-05-12 Created: 2016-05-12 Last updated: 2017-11-30
Johnsson, M., Gering, E., Willis, P., Lopez, S., Van Dorp, L., Hellenthal, G., . . . Wright, D. (2016). Feralisation targets different genomic loci to domestication in the chicken.. Nature Communications, 7, Article ID 12950.
Open this publication in new window or tab >>Feralisation targets different genomic loci to domestication in the chicken.
Show others...
2016 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 7, article id 12950Article in journal (Refereed) Published
Abstract [en]

Feralisation occurs when a domestic population recolonizes the wild, escaping its previous restricted environment, and has been considered as the reverse of domestication. We have previously shown that Kauai Island's feral chickens are a highly variable and admixed population. Here we map selective sweeps in feral Kauai chickens using whole-genome sequencing. The detected sweeps were mostly unique to feralisation and distinct to those selected for during domestication. To ascribe potential phenotypic functions to these genes we utilize a laboratory-controlled equivalent to the Kauai population-an advanced intercross between Red Junglefowl and domestic layer birds that has been used previously for both QTL and expression QTL studies. Certain sweep genes exhibit significant correlations with comb mass, maternal brooding behaviour and fecundity. Our analyses indicate that adaptations to feral and domestic environments involve different genomic regions and feral chickens show some evidence of adaptation at genes associated with sexual selection and reproduction.

Place, publisher, year, edition, pages
London: Nature Publishing Group, 2016
National Category
Genetics
Identifiers
urn:nbn:se:liu:diva-122279 (URN)10.1038/ncomms12950 (DOI)000385444300002 ()27686863 (PubMedID)
Note

The prevous status of this article was Manuscript and the title was The genomic signals of feralisation: Not just domestication in reverse?

Funding agencies: We thank Tony Lydgate and the Steelgrass Institute for invaluable assistance and accommodation on Kauai. The research was carried out within the framework of the Linkoping University Neuro-network. WGS was performed by the Uppsala Genome Center as part of NGI Sweden. Computations were performed at UPPMAX as part of SNIC Sweden. The project was supported by grants from the Swedish Research Council (VR), the Swedish Research Council for Environment, Agricultural Sciences and Spatial Planning (FORMAS), the Carl Trygers Stiftelse and by the National Science Foundation under Cooperative Agreement No. DBI-0939454. S.L. is supported by BBSRC (grant number BB/L009382/1). L.V.D. is supported by CoMPLEX via EPSRC (grant number EP/F500351/1). G.H. is supported by a Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (grant number 098386/Z/12/Z) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. Any opinions, findings and conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of the National Science Foundation.

Available from: 2015-10-27 Created: 2015-10-27 Last updated: 2017-12-01Bibliographically approved
Rice, W., Friberg, U. & Gavrilets, S. (2016). Sexually antagonistic epigenetic marks that canalize sexually dimorphic development. Molecular Ecology, 25(8), 1812-1822
Open this publication in new window or tab >>Sexually antagonistic epigenetic marks that canalize sexually dimorphic development
2016 (English)In: Molecular Ecology, ISSN 0962-1083, E-ISSN 1365-294X, Vol. 25, no 8, p. 1812-1822Article in journal (Refereed) Published
Abstract [en]

The sexes share the same autosomal genomes, yet sexual dimorphism is common due to sex-specific gene expression. When present, XX and XY karyotypes trigger alternate regulatory cascades that determine sex-specific gene expression profiles. In mammals, secretion of testosterone (T) by the testes during foetal development is the master switch influencing the gene expression pathways (male vs. female) that will be followed, but many genes have sex-specific expression prior to T secretion. Environmental factors, like endocrine disruptors and mimics, can interfere with sexual development. However, sex-specific ontogeny can be canalized by the production of epigenetic marks (epimarks) generated during early ontogeny that increase sensitivity of XY embryos to T and decrease sensitivity of XX embryos. Here, we integrate and synthesize the evidence indicating that canalizing epimarks are produced during early ontogeny. We will also describe the evidence that such epimarks sometimes carry over across generations and produce mosaicism in which some traits are discordant with the gonad. Such carryover epimarks are sexually antagonistic because they benefit the individual in which they were formed (via canalization) but harm opposite-sex offspring when they fail to erase across generations and produce gonad-trait discordances. SA-epimarks have the potential to: i) magnify phenotypic variation for many sexually selected traits, ii) generate overlap along many dimensions of the masculinity/femininity spectrum, and iii) influence medically important gonad-trait discordances like cryptorchidism, hypospadias and idiopathic hirsutism.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2016
Keywords
sexual dimorphism, canalization, sexual conflict, gonad-trait discordance, epigenetics
National Category
Genetics
Identifiers
urn:nbn:se:liu:diva-128119 (URN)10.1111/mec.13490 (DOI)000374776300014 ()26600375 (PubMedID)
Note

Funding agencies: National Science Foundation [DBI-1300426]; University of Tennessee, Knoxville; Swedish Foundation for Strategic Research

Available from: 2016-05-17 Created: 2016-05-17 Last updated: 2017-11-30Bibliographically approved
Friberg, U. (2016). Två kön och många organ: men bara en arvsmassa. Tidskriften för svensk psykiatri (4), 28-29
Open this publication in new window or tab >>Två kön och många organ: men bara en arvsmassa
2016 (Swedish)In: Tidskriften för svensk psykiatri, ISSN 1653-8579, no 4, p. 28-29Article in journal (Other academic) Published
Abstract [sv]

Hos många arter uppvisar könen en rad skillnader.Dessa omfattar vanligtvis deras utseende så väl som beteende. Vad är det egentligen som orsakar evolution av könsskillnader, hur är den möjlig då könen har i princip samma gener, och kan detta tänkas ha konsekvenser för hur vi människor fungerar?

Place, publisher, year, edition, pages
Svenska Psykiatriska Föreningen, Svenska Föreningen för Barn- och Ungdomspsykiatri och Svenska Rättspsykiatriska Föreningen, 2016
National Category
Biological Sciences Genetics
Identifiers
urn:nbn:se:liu:diva-137278 (URN)
Available from: 2017-05-10 Created: 2017-05-10 Last updated: 2017-05-19Bibliographically approved
Stocks, M., Dean, R., Rogell, B. & Friberg, U. (2015). Sex-specific Trans-regulatory Variation on the Drosophila melanogaster X Chromosome. PLoS Genetics, 11(2), 1-19, Article ID e1005015.
Open this publication in new window or tab >>Sex-specific Trans-regulatory Variation on the Drosophila melanogaster X Chromosome
2015 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 11, no 2, p. 1-19, article id e1005015Article in journal (Refereed) Published
Abstract [en]

The X chromosome constitutes a unique genomic environment because it is present in onecopy in males, but two copies in females. This simple fact has motivated several theoreticalpredictions with respect to how standing genetic variation on the X chromosome should differfrom the autosomes. Unmasked expression of deleterious mutations in males and alower census size are expected to reduce variation, while allelic variants with sexually antagonisticeffects, and potentially those with a sex-specific effect, could accumulate on theX chromosome and contribute to increased genetic variation. In addition, incomplete dosagecompensation of the X chromosome could potentially dampen the male-specific effectsof random mutations, and promote the accumulation of X-linked alleles with sexually dimorphicphenotypic effects. Here we test both the amount and the type of genetic variation onthe X chromosome within a population of Drosophila melanogaster, by comparing the proportionof X linked and autosomal trans-regulatory SNPs with a sexually concordant anddiscordant effect on gene expression. We find that the X chromosome is depleted for SNPswith a sexually concordant effect, but hosts comparatively more SNPs with a sexually discordanteffect. Interestingly, the contrasting results for SNPs with sexually concordant anddiscordant effects are driven by SNPs with a larger influence on expression in females thanexpression in males. Furthermore, the distribution of these SNPs is shifted towards regionswhere dosage compensation is predicted to be less complete. These results suggest thatintrinsic properties of dosage compensation influence either the accumulation of differenttypes of trans-factors and/or their propensity to accumulate mutations. Our findings documenta potential mechanistic basis for sex-specific genetic variation, and identify the X as areservoir for sexually dimorphic phenotypic variation. These results have general implicationsfor X chromosome evolution, as well as the genetic basis of sex-specificevolutionary change.

National Category
Evolutionary Biology
Identifiers
urn:nbn:se:liu:diva-117546 (URN)10.1371/journal.pgen.1005015 (DOI)000352081800062 ()25679222 (PubMedID)
Available from: 2015-05-04 Created: 2015-05-04 Last updated: 2017-12-04
Pischedda, A., Friberg, U., Stewart, A. D., Miller, P. M. & Rice, W. R. (2015). Sexual selection has minimal impact on effective population sizes in species with high rates of random offspring mortality: An empirical demonstration using fitness distributions. Evolution, 69(10), 2638-2647
Open this publication in new window or tab >>Sexual selection has minimal impact on effective population sizes in species with high rates of random offspring mortality: An empirical demonstration using fitness distributions
Show others...
2015 (English)In: Evolution, ISSN 0014-3820, E-ISSN 1558-5646, Vol. 69, no 10, p. 2638-2647Article in journal (Refereed) Published
Abstract [en]

The effective population size (N-e) is a fundamental parameter in population genetics that influences the rate of loss of genetic diversity. Sexual selection has the potential to reduce N-e by causing the sex-specific distributions of individuals that successfully reproduce to diverge. To empirically estimate the effect of sexual selection on N-e, we obtained fitness distributions for males and females from an outbred, laboratory-adapted population of Drosophila melanogaster. We observed strong sexual selection in this population (the variance in male reproductive success was approximate to 14 times higher than that for females), but found that sexual selection had only a modest effect on N-e, which was 75% of the census size. This occurs because the substantial random offspring mortality in this population diminishes the effects of sexual selection on N-e, a result that necessarily applies to other high fecundity species. The inclusion of this random offspring mortality creates a scaling effect that reduces the variance/mean ratios for male and female reproductive success and causes them to converge. Our results demonstrate that measuring reproductive success without considering offspring mortality can underestimate N-e and overestimate the genetic consequences of sexual selection. Similarly, comparing genetic diversity among different genomic components may fail to detect strong sexual selection.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2015
Keywords
Autosomes; genetic variation; juvenile mortality; reproductive success; selection; sex chromosomes
National Category
Biological Sciences
Identifiers
urn:nbn:se:liu:diva-122530 (URN)10.1111/evo.12764 (DOI)000362970600009 ()26374275 (PubMedID)
Note

Funding Agencies|Sigma Xi; UCSB; National Science Foundation [DEB-0128780, DEB-0111613, DBI-0409561]; National Institutes of Health [R01HD057974-01]; Natural Sciences and Engineering Research Council of Canada; Swedish Research Council

Available from: 2015-11-09 Created: 2015-11-06 Last updated: 2017-12-01
Friberg, U. & Rice, W. R. (2015). Sexually Antagonistic Zygotic Drive: A New Form of Genetic Conflict between the Sex Chromosomes. Cold Spring Harbor Perspectives in Biology, 7(3), a017608
Open this publication in new window or tab >>Sexually Antagonistic Zygotic Drive: A New Form of Genetic Conflict between the Sex Chromosomes
2015 (English)In: Cold Spring Harbor Perspectives in Biology, ISSN 1943-0264, E-ISSN 1943-0264, Vol. 7, no 3, p. a017608-Article in journal (Refereed) Published
Abstract [en]

Sisters and brothers are completely unrelated with respect to the sex chromosomes they inherit from their heterogametic parent. This has the potential to result in a previously unappreciated form of genetic conflict between the sex chromosomes, called sexually antagonistic zygotic drive (SA-ZD). SA-ZD can arise whenever brothers and sisters compete over limited resources or there is brother-sister mating coupled with inbreeding depression. Although theory predicts that SA-ZD should be common and influence important evolutionary processes, there is little empirical evidence for its existence. Here we discuss the current understanding of SA-ZD, why it would be expected to elude empirical detection when present, and how it relates to other forms of genetic conflict.

Place, publisher, year, edition, pages
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT, 2015
National Category
Biological Sciences
Identifiers
urn:nbn:se:liu:diva-116956 (URN)10.1101/cshperspect.a017608 (DOI)000351205300007 ()25573714 (PubMedID)2-s2.0-84923920267 (Scopus ID)
Note

Funding Agencies|Swedish Research Council; Swedish Foundation for Strategic Research

Available from: 2015-04-13 Created: 2015-04-10 Last updated: 2017-12-04
Maklakov, A. A., Rowe, L. & Friberg, U. (2015). Why organisms age: Evolution of senescence under positive pleiotropy?. Bioessays, 37(7), 802-807
Open this publication in new window or tab >>Why organisms age: Evolution of senescence under positive pleiotropy?
2015 (English)In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 37, no 7, p. 802-807Article in journal (Refereed) Published
Abstract [en]

Two classic theories maintain that aging evolves eitherbecause of alleles whose deleterious effects are confinedto late life or because of alleles with broad pleiotropiceffects that increase early-life fitness at the expense oflate-life fitness. However, empirical studies often revealpositive pleiotropy for fitness across age classes, andrecent evidence suggests that selection on early-lifefitness can decelerate aging and increase lifespan, therebycasting doubt on the current consensus. Here, we brieflyreview these data and promote the simple argument thataging can evolve under positive pleiotropy between earlyandlate-life fitness when the deleterious effect ofmutations increases with age. We argue that thishypothesis makes testable predictions and is supportedby existing evidence.

Place, publisher, year, edition, pages
Wiley Periodicals, Inc., 2015
Keywords
Aging; life-history evolution; mutation accumulation; positive pleiotropy; senescence
National Category
Evolutionary Biology
Identifiers
urn:nbn:se:liu:diva-117545 (URN)10.1002/bies.201500025 (DOI)000356827700012 ()25900580 (PubMedID)
Available from: 2015-05-04 Created: 2015-05-04 Last updated: 2017-12-04
Griffin, R. M., Le Gall, D., Schielzeth, H. & Friberg, U. (2015). Within-population Y-linked genetic variation for lifespan in Drosophila melanogaster. Journal of Evolutionary Biology, 28(11), 1940-1947
Open this publication in new window or tab >>Within-population Y-linked genetic variation for lifespan in Drosophila melanogaster
2015 (English)In: Journal of Evolutionary Biology, ISSN 1010-061X, E-ISSN 1420-9101, Vol. 28, no 11, p. 1940-1947Article in journal (Refereed) Published
Abstract [en]

The view that the Y chromosome is of little importance for phenotypic evolution stems from early studies of Drosophila melanogaster. This species Y chromosome contains only 13 protein-coding genes, is almost entirely heterochromatic and is not necessary for male viability. Population genetic theory further suggests that non-neutral variation can only be maintained at the Y chromosome under special circumstances. Yet, recent studies suggest that the D.melanogaster Y chromosome trans-regulates hundreds to thousands of X and autosomal genes. This finding suggests that the Y chromosome may play a far more active role in adaptive evolution than has previously been assumed. To evaluate the potential for the Y chromosome to contribute to phenotypic evolution from standing genetic variation, we test for Y-linked variation in lifespan within a population of D.melanogaster. Assessing variation for lifespan provides a powerful test because lifespan (i) shows sexual dimorphism, which the Y is primarily predicted to contribute to, (ii) is influenced by many genes, which provides the Y with many potential regulatory targets and (iii) is sensitive to heterochromatin remodelling, a mechanism through which the Y chromosome is believed to regulate gene expression. Our results show a small but significant effect of the Y chromosome and thus suggest that the Y chromosome has the potential to respond to selection from standing genetic variation. Despite its small effect size, Y-linked variation may still be important, in particular when evolution of sexual dimorphism is genetically constrained elsewhere in the genome.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2015
Keywords
intralocus sexual conflict; longevity; sex chromosomes; sexual dimorphism; Y chromosome
National Category
Biological Sciences
Identifiers
urn:nbn:se:liu:diva-123149 (URN)10.1111/jeb.12708 (DOI)000364641900003 ()26230387 (PubMedID)
Note

Funding Agencies|Swedish Foundation for Strategic Research; Carl Tryggers Foundation; Swedish Research Council; German Research Foundation (DFG) [SCHI 1188/1-1]

Available from: 2015-12-07 Created: 2015-12-04 Last updated: 2017-12-01
Maklakov, A. A., Immler, S., Løvlie, H., Flis, I. & Friberg, U. (2013). The effect of sexual harassment on lethal mutation rate in female Drosophila melanogaster. Proceedings of the Royal Society of London. Biological Sciences, 280(1750)
Open this publication in new window or tab >>The effect of sexual harassment on lethal mutation rate in female Drosophila melanogaster
Show others...
2013 (English)In: Proceedings of the Royal Society of London. Biological Sciences, ISSN 0962-8452, E-ISSN 1471-2954, Vol. 280, no 1750Article in journal (Refereed) Published
Abstract [en]

The rate by which new mutations are introduced into a population may have far-reaching implications for processes at the population level. Theory assumes that all individuals within a population have the same mutation rate, but this assumption may not be true. Compared with individuals in high condition, those in poor condition may have fewer resources available to invest in DNA repair, resulting in elevated mutation rates. Alternatively, environmentally induced stress can result in increased investment in DNA repair at the expense of reproduction. Here, we directly test whether sexual harassment by males, known to reduce female condition, affects female capacity to alleviate DNA damage in Drosophila melanogaster fruitflies. Female gametes can repair double-strand DNA breaks in sperm, which allows manipulating mutation rate independently from female condition. We show that male harassment strongly not only reduces female fecundity, but also reduces the yield of dominant lethal mutations, supporting the hypothesis that stressed organisms invest relatively more in repair mechanisms. We discuss our results in the light of previous research and suggest that social effects such as density and courtship can play an important and underappreciated role in mediating condition-dependent mutation rate.

Place, publisher, year, edition, pages
London, UK: Royal Society, 2013
Keywords
hormesis, mutation rate, sexual conflict, sexual selection
National Category
Evolutionary Biology
Identifiers
urn:nbn:se:liu:diva-111367 (URN)10.1098/rspb.2012.1874 (DOI)000311943100004 ()23173200 (PubMedID)
Available from: 2014-10-15 Created: 2014-10-15 Last updated: 2017-12-05Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-6112-9586

Search in DiVA

Show all publications