98%
921
2 minutes
20
Background: Birds of prey (raptors) are dominant apex predators in terrestrial communities, with hawks (Accipitriformes) and falcons (Falconiformes) hunting by day and owls (Strigiformes) hunting by night.
Results: Here, we report new genomes and transcriptomes for 20 species of birds, including 16 species of birds of prey, and high-quality reference genomes for the Eurasian eagle-owl (Bubo bubo), oriental scops owl (Otus sunia), eastern buzzard (Buteo japonicus), and common kestrel (Falco tinnunculus). Our extensive genomic analysis and comparisons with non-raptor genomes identify common molecular signatures that underpin anatomical structure and sensory, muscle, circulatory, and respiratory systems related to a predatory lifestyle. Compared with diurnal birds, owls exhibit striking adaptations to the nocturnal environment, including functional trade-offs in the sensory systems, such as loss of color vision genes and selection for enhancement of nocturnal vision and other sensory systems that are convergent with other nocturnal avian orders. Additionally, we find that a suite of genes associated with vision and circadian rhythm are differentially expressed in blood tissue between nocturnal and diurnal raptors, possibly indicating adaptive expression change during the transition to nocturnality.
Conclusions: Overall, raptor genomes show genomic signatures associated with the origin and maintenance of several specialized physiological and morphological features essential to be apex predators.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6714440 | PMC |
http://dx.doi.org/10.1186/s13059-019-1793-1 | DOI Listing |
Zoonoses Public Health
September 2025
Departamento de Sanidad Animal, Grupo de Investigación en Sanidad Animal y Zoonosis (GISAZ), UIC Zoonosis y Enfermedades Emergentes ENZOEM, Universidad de Córdoba, Córdoba, Spain.
We report mortality in bearded vultures ( Gypaetus barbatus ) associated with highly pathogenic avian influenza HPAI A H5N1 clade 2.3.4.
View Article and Find Full Text PDFBMC Ecol Evol
July 2025
Wildlife Research Center, Kyoto University, Kyoto, Japan.
Prey species often develop toxic chemical defenses against predators, prompting predators to evolve traits that counteract these toxins. A prime example of this evolutionary arms race involves resistance to lethal cardiotonic steroids, which is associated with specific amino acid mutations in the α-subunit of Na+/K+-ATPase (ATP1A) across diverse predator species. The Japanese Crested Serpent-eagle (Spilornis cheela perplexus), which is endemic to the adjacent islands of Ishigaki and Iriomote in Okinawa, provides an intriguing example of this convergent evolution.
View Article and Find Full Text PDFVet Res Commun
July 2025
School of Veterinary Medicine, Metropolitan University of Santos, Santos, Brazil.
The dissemination of extended-spectrum β-lactamase (ESBL)-producing Enterbacterales, once largely confined to healthcare settings, has become a growing One Health concern as these pathogens threaten diverse environments, including wildlife habitats. This study describes high-risk clones of ESBL-producing Enterobacterales in wildlife undergoing rehabilitation at a zoological park in Southeast Brazil. Among 49 wild mammals and birds sampled, two Escherichia coli strains, from a rusty-barred owl and a black vulture, tested positive for ESBL production and exhibited multidrug resistance profiles.
View Article and Find Full Text PDFmBio
August 2025
Research Unit Marine Symbioses, GEOMAR Helmholtz Centre for Ocean Research Kiel, Kiel, Germany.
Unlabelled: Phagocytosis is a conserved cellular mechanism for food uptake, defense, and animal-microbe interactions in metazoans. How the discrimination and subsequent processing of different microbes in marine invertebrates is facilitated remains largely unknown. Thereto, we combined a recently developed phagocytic assay with proteomics analysis to compare the phagocytic activity of the sponge upon encounter with the native Hal 281 (i.
View Article and Find Full Text PDFAn inherited, expanded CAG repeat in HTT undergoes further somatic expansion to cause Huntington's disease (HD). To gain insights into this molecular mechanism, we compared genome-wide association studies of somatic expansion in blood and somatic expansion-driven HD clinical phenotypes. Here, we show that somatic expansion is driven by a mismatch repair-related process whose genetic modification and consequences show unexpected complexity, including cell-type specificity.
View Article and Find Full Text PDF