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Identifying the mechanisms of phenotypic robustness using fluctuating asymmetry

Project description

Investigating phenotypic robustness based on fluctuating asymmetry

Phenotypic robustness is essential for an organism’s evolutionary success and biological stability. Yet, little is known of the mechanisms behind it. Supported by the Marie Skłodowska-Curie Actions programme, the SymFish project will explore the mechanisms of phenotypic robustness based on fluctuating asymmetry. To do so, it will observe the ongoing hybridisation of cichlid fish, whose offspring display elevated rates of left-right colour pattern asymmetry as opposed to their symmetrical parents. The study aims to gain insight into how phenotypic robustness works by identifying the extent to which it is inheritable, testing gene-environment interactions to determine whether similar mechanisms control intrinsic and extrinsic robustness, and measuring asymmetry in other traits to decipher whether robustness is correlated across organ systems.

Objective

Phenotypic robustness, the capacity for organisms to buffer their development against internal and external perturbations, controls the strength of the links between phenotypes, genotypes, and environments. Despite its importance linking scales of biological organization, we have a poor understanding of how phenotypic robustness works—for example, the degree to which it is heritable, if the same mechanisms control both intrinsic and extrinsic robustness, or if it is correlated across organ systems. Working with Dr. Claudius Kratochwil in the Integrated Evolutionary Biology group at the University of Helsinki (UH), Finland, I will investigate the mechanisms of robustness using fluctuating asymmetry as an indicator of robustness. I will take advantage an ongoing hybrid cross of cichlid fishes in the lab, the offspring of which exhibit increasing rates of left-right color pattern asymmetry compared to their symmetrical parents. In research objective O1, I will identify the genomic basis of phenotypic robustness by selecting for increased and decreased color pattern asymmetry in this hybrid cross, and use whole genome sequencing to identify loci associated with decreased symmetry. In O2, I will test for gene-environment interactions in robustness by raising fish from asymmetrical and symmetrical populations at high and low temperatures and testing whether these populations exhibit different reaction norms. In O3, I will test whether robustness is correlated across organ systems by measuring asymmetry in other traits (paired fins, gills, jaws, eyes, and lateral line neuromasts) in the most and least asymmetrical fish from the cross. I will ask whether selecting for asymmetry in color patterns has also increased asymmetry in these traits.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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(opens in new window) HORIZON-MSCA-2024-PF-01

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Coordinator

HELSINGIN YLIOPISTO
Net EU contribution

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€ 226 276,80
Address
FABIANINKATU 33
00014 HELSINGIN YLIOPISTO
Finland

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Activity type
Higher or Secondary Education Establishments
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Total cost

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