English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Intra-species differences in population size shape life history and genome evolution

MPS-Authors
/persons/resource/persons281156

Willemsen,  D.
Valenzano – Evolutionary and Experimental Biology of Ageing, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

/persons/resource/persons278154

Cui,  R.
Valenzano – Evolutionary and Experimental Biology of Ageing, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

/persons/resource/persons278157

Valenzano,  D. R.
Valenzano – Evolutionary and Experimental Biology of Ageing, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Willemsen, D., Cui, R., Reichard, M., & Valenzano, D. R. (2020). Intra-species differences in population size shape life history and genome evolution. Elife, 9. doi:10.7554/eLife.55794.


Cite as: https://hdl.handle.net/21.11116/0000-000B-2DDE-A
Abstract
The evolutionary forces shaping life history divergence within species are largely unknown. Turquoise killifish display differences in lifespan among wild populations, representing an ideal natural experiment in evolution and diversification of life history. By combining genome sequencing and population genetics, we investigate the evolutionary forces shaping lifespan among wild turquoise killifish populations. We generate an improved reference genome assembly and identify genes under positive and purifying selection, as well as those evolving neutrally. Short-lived populations from the outer margin of the species range have small population size and accumulate deleterious mutations in genes significantly enriched in the WNT signaling pathway, neurodegeneration, cancer and the mTOR pathway. We propose that limited population size due to habitat fragmentation and repeated population bottlenecks, by increasing the genome-wide mutation load, exacerbates the effects of mutation accumulation and cumulatively contribute to the short adult lifespan.