English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Gene losses in the common vampire bat illuminate molecular adaptations to blood feeding.

MPS-Authors
/persons/resource/persons246904

Pippel,  Martin
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

Jebb,  David
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons222079

Hecker,  Nikolai
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons219312

Kirilenko,  Bogdan
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons184581

Hiller,  Michael
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

External Resource
No external resources are shared
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

Blumer, M., Brown, T., Freitas, M. B., Destro, A. L., Oliveira, J. A., Morales, A. E., et al. (2022). Gene losses in the common vampire bat illuminate molecular adaptations to blood feeding. Science advances, 8(12): eabm6494. doi:10.1126/sciadv.abm6494.


Cite as: https://hdl.handle.net/21.11116/0000-000B-034B-E
Abstract
Vampire bats are the only mammals that feed exclusively on blood. To uncover genomic changes associated with this dietary adaptation, we generated a haplotype-resolved genome of the common vampire bat and screened 27 bat species for genes that were specifically lost in the vampire bat lineage. We found previously unknown gene losses that relate to reduced insulin secretion (FFAR1 and SLC30A8), limited glycogen stores (PPP1R3E), and a unique gastric physiology (CTSE). Other gene losses likely reflect the biased nutrient composition (ERN2 and CTRL) and distinct pathogen diversity of blood (RNASE7) and predict the complete lack of cone-based vision in these strictly nocturnal bats (PDE6H and PDE6C). Notably, REP15 loss likely helped vampire bats adapt to high dietary iron levels by enhancing iron excretion, and the loss of CYP39A1 could have contributed to their exceptional cognitive abilities. These findings enhance our understanding of vampire bat biology and the genomic underpinnings of adaptations to blood feeding.