A refined model of the genomic basis for phenotypic variation in vertebrate hemostasis.
Abstract
BACKGROUND: Hemostasis is a defense mechanism that enhances an organism's survival
by minimizing blood loss upon vascular injury. In vertebrates, hemostasis has been
evolving with the cardio-vascular and hemodynamic systems over the last 450 million
years. Birds and mammals have very similar vascular and hemodynamic systems, thus
the mechanism that blocks ruptures in the vasculature is expected to be the same.
However, the speed of the process varies across vertebrates, and is particularly slow
for birds. Understanding the differences in the hemostasis pathway between birds and
mammals, and placing them in perspective to other vertebrates may provide clues to
the genetic contribution to variation in blood clotting phenotype in vertebrates.
We compiled genomic data corresponding to key elements involved in hemostasis across
vertebrates to investigate its genetic basis and understand how it affects fitness.
RESULTS: We found that: i) fewer genes are involved in hemostasis in birds compared
to mammals; and ii) the largest differences concern platelet membrane receptors and
components from the kallikrein-kinin system. We propose that lack of the cytoplasmic
domain of the GPIb receptor subunit alpha could be a strong contributor to the prolonged
bleeding phenotype in birds. Combined analysis of laboratory assessments of avian
hemostasis with the first avian phylogeny based on genomic-scale data revealed that
differences in hemostasis within birds are not explained by phylogenetic relationships,
but more so by genetic variation underlying components of the hemostatic process,
suggestive of natural selection. CONCLUSIONS: This work adds to our understanding
of the evolution of hemostasis in vertebrates. The overlap with the inflammation,
complement and renin-angiotensin (blood pressure regulation) pathways is a potential
driver of rapid molecular evolution in the hemostasis network. Comparisons between
avian species and mammals allowed us to hypothesize that the observed mammalian innovations
might have contributed to the diversification of mammals that give birth to live young.
Type
Journal articleSubject
AnimalsBiological Evolution
Birds
Blood Coagulation Factors
Evolution, Molecular
Genetic Variation
Hemostasis
Phylogeny
Selection, Genetic
Vertebrates
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https://hdl.handle.net/10161/11124Published Version (Please cite this version)
10.1186/s12862-015-0409-yPublication Info
Ribeiro, Ângela M; Zepeda-Mendoza, M Lisandra; Bertelsen, Mads F; Kristensen, Annemarie
T; Jarvis, Erich D; Gilbert, M Thomas P; & da Fonseca, Rute R (2015). A refined model of the genomic basis for phenotypic variation in vertebrate hemostasis.
BMC Evol Biol, 15. pp. 124. 10.1186/s12862-015-0409-y. Retrieved from https://hdl.handle.net/10161/11124.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Erich David Jarvis
Adjunct Professor in the Deptartment of Neurobiology
Dr. Jarvis' laboratory studies the neurobiology of vocal communication. Emphasis is
placed on the molecular pathways involved in the perception and production of learned
vocalizations. They use an integrative approach that combines behavioral, anatomical,
electrophysiological and molecular biological techniques. The main animal model used
is songbirds, one of the few vertebrate groups that evolved the ability to learn vocalizations.
The generality of the discoveries is tested in other vocal lear

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