Axel WibergResearcher
About me
I am evolutionary biologist with a broad interest in understanding the genetic basis of adaptations.
I have a particular interest in sexual selection and conflict and I apply the tools methods of modern genomics to try to understand how these forces drive evolutionary change.
Currently my research focuses on:
- Sexually antagonistic coevolution at the molecular level using the sex-peptide network in D. melanogaster as a model system. This work also includes with isofemale lines from several european populations
- Signals of local adaptation to ecology at SFP (Seminal Fluid Protein) loci in D. melanogaster.
I'm also involved in several other projects on adaptation genomics in various systems.
If these topics interest you, then please get in touch!
I am always happy to discuss B.Sc. and M.Sc. thesis projects ideas.
Publications
A selection from Stockholm University publication database
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Y-Linked Copy Number Polymorphism of Target of Rapamycin Is Associated with Sexual Size Dimorphism in Seed Beetles
2023. Philipp Kaufmann (et al.). Molecular biology and evolution 40 (8)
ArticleRead more about Y-Linked Copy Number Polymorphism of Target of Rapamycin Is Associated with Sexual Size Dimorphism in Seed BeetlesThe Y chromosome is theorized to facilitate evolution of sexual dimorphism by accumulating sexually antagonistic loci, but empirical support is scarce. Due to the lack of recombination, Y chromosomes are prone to degenerative processes, which poses a constraint on their adaptive potential. Yet, in the seed beetle, Callosobruchus maculatus segregating Y linked variation affects male body size and thereby sexual size dimorphism (SSD). Here, we assemble C. maculatus sex chromosome sequences and identify molecular differences associated with Y-linked SSD variation. The assembled Y chromosome is largely euchromatic and contains over 400 genes, many of which are ampliconic with a mixed autosomal and X chromosome ancestry. Functional annotation suggests that the Y chromosome plays important roles in males beyond primary reproductive functions. Crucially, we find that, besides an autosomal copy of the gene target of rapamycin (TOR), males carry an additional TOR copy on the Y chromosome. TOR is a conserved regulator of growth across taxa, and our results suggest that a Y-linked TOR provides a male specific opportunity to alter body size. A comparison of Y haplotypes associated with male size difference uncovers a copy number variation for TOR, where the haplotype associated with decreased male size, and thereby increased sexual dimorphism, has two additional TOR copies. This suggests that sexual conflict over growth has been mitigated by autosome to Y translocation of TOR followed by gene duplications. Our results reveal that despite of suppressed recombination, the Y chromosome can harbor adaptive potential as a male-limited supergene.
Show all publications by Axel Wiberg at Stockholm University