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- Arnqvist, Lisa, 1970-, et al.
(författare)
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Overexpression of CYP710A1 and CYP710A4 in transgenic Arabidopsis plants increases the level of stigmasterol at the expense of sitosterol
- 2008
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Ingår i: Planta. - : Springer Science and Business Media LLC. - 0032-0935 .- 1432-2048. ; 227:2, s. 309-317
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Tidskriftsartikel (refereegranskat)abstract
- Sitosterol and stigmasterol are major sterols in vascular plants. An altered stigmasterol:sitosterol ratio has been proposed to influence the properties of cell membranes, particularly in relation to various stresses, but biosynthesis of stigmasterol is poorly understood. Recently, however, Morikawa et al. (Plant Cell 18:1008–1022, 2006) showed in Arabidopsis thaliana that synthesis of stigmasterol and brassicasterol is catalyzed by two separate sterol C-22 desaturases, encoded by the genes CYP710A1 and CYP710A2, respectively. The proteins belong to a small cytochrome P450 subfamily having four members, denoted by CYP710A1-A4, and are related to the yeast sterol C-22 desaturase Erg5p acting in ergosterol synthesis. Here, we report on our parallel investigation of the Arabidopsis CYP710A family. To elucidate the function of CYP710A proteins, transgenic Arabidopsis plants were generated overexpressing CYP710A1 and CYP710A4. Compared to wild-type plants, both types of transformant displayed a normal phenotype, but contained increased levels of free stigmasterol and a concomitant decrease in the level of free sitosterol. CYP710A1 transformants also displayed higher levels of esterified forms of stigmasterol, cholesterol, 24-methylcholesterol and isofucosterol. The results confirm the findings of Morikawa et al. (Plant Cell 18:1008–1022, 2006) regarding the function of CYP710A1 in stigmasterol synthesis, and show that CYP710A4 also has this capacity. Furthermore, our results suggest that an increased stigmasterol level alone is sufficient to stimulate esterification of other major sterols.
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- Siljestam, Mattias, 1989-
(författare)
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Mathematical Solutions to Divergent Evolution
- 2024
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Diversity is ubiquitous in nature and manifests through various forms of divergent evolution. Using mathematical models that consider the interplay between ecology and evolution, I explore mechanisms driving two types of such divergence: the emergence of genetic diversity in diploid organisms, and the initial sexual dimorphism of anisogamy.Genetic diversity is typically studied as a consequence of competition or local adaptation. However, diploidy introduces an alternative mechanism: heterozygote advantage (HA), where alleles provide complementary functionalities. A classical example is the immune genes of the Major Histocompatibility Complex (MHC), where alleles can protect against complementary sets of pathogens. HA can emerge if individuals encounter multiple pathogens. When pathogens are distributed over habitats, divergence can be driven by local adaptation, or an emerging HA if migration is high. Alternatively, if MHC alleles provide full defence as a single copy (adaptive context-specific dominance), HA can also emerge under low migration. I challenge the view that HA alone cannot explain the high polymorphism observed at MHC loci by demonstrating that over 100 alleles can be maintained based on two critical assumptions: pathogens can be lethal if not properly countered by an immune response, and the combined effect of multiple pathogens can exceed the sum of their individual impacts.For loci under sexually antagonistic selection, divergent evolution can facilitate the coexistence of alleles, each producing a homozygote genotype with an optimal phenotype in one sex while the heterozygote exhibits an intermediate maladapted phenotype. However, I show that sex-specific dominance is expected to evolve, resulting in a marginal HA across the sexes: a heterozygote carrying alleles optimal for each sex exhibits an optimal phenotype in both sexes, whereas the corresponding homozygotes are maladapted in one sex. This leads to further divergence and the coexistence of many alleles, for wide parameter ranges.Additionally, I challenge the traditional view that male-biased competition for mating is an inevitable consequence of anisogamy---the evolutionary differentiation in gamete size between the sexes. I present the first theoretical description of the coevolution of anisogamy and mating competition, demonstrating that anisogamy does not inherently favour male competition. Instead, the specific evolutionary conditions and the nature of the competition trait significantly influence which sex invests more in mating competition.This thesis not only enhances our understanding of the underlying drivers of genetic and phenotypic diversity but also challenges longstanding evolutionary paradigms, shedding light on the complex dynamics that shape life’s vast diversity.
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- Siljestam, Mattias, 1989-, et al.
(författare)
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Sex-specific Dominance and Its Effects on Allelic Diversity in Sexually Antagonistic Loci
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Sexually antagonistic (SA) selection, favouring different alleles in males and females, can contribute to the maintenance of genetic diversity. While current theory predicts that biallelic polymorphism can be maintained in SA loci, particularly with strong selection or sex-specific dominance, some candidate SA loci harbour more than two segregating alleles. This highlights a gap in our understanding of the origin and maintenance of SA genetic variation. We present a mathematical model to explore the evolution of alleles at either an autosomal or an X-linked locus under SA selection, affecting a quantitative trait with distinct female and male optima. We find that polyallelic polymorphism can evolve under conditions of sex-specific or X-linked dominance for the trait, particularly under weak selection, such that several alleles coexist in a single population through balancing selection. We show that additive allelic effects predict only biallelic polymorphism, and only under symmetric and relatively strong selection. However, our analysis also shows that sex-specific dominance (and X-linked dominance) evolves when permitted, which promotes the evolution of polyallelic polymorphism and reduces the gender load. We conclude that SA selection can drive the co-evolution of sex-specific dominance and polyallelic polymorphism, particularly under weak selection. To assess these findings, we analyse segregating variation in three populations of a seed beetle model system and find support for our predictions: (i) candidate SA loci show a relatively strong signal of polyallelic polymorphism and (ii) loci with the strongest signal of polyallelic polymorphism are enriched with genes associated with known SA phenotypes.
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