Biology subjects

Alves, J.

Publications and source records attributed to Alves, J..

15 recordsLinked to original sources

bioRxiv2026

ARTIFICIAL SELECTION DIVERSIFIES BIRDSONG THROUGH POLYGENIC CHANGES ACROSS SENSORY AND MOTOR SYSTEMS

Vocal learning, or the ability to acquire and produce contextualized sounds through social interaction, underlies human speech yet has evolved in a few animal lineages, including songbirds. In songbirds, learned song is produced by a dedicated neural circuit and depends on auditory feedback for its acquisition and maintenance. Roughly four centuries of artificial selection on the domestic canary (Serinus canaria) have produced song breeds whose vocalizations diverge as much as those of distinct species, offering a rare intraspecific system in which to identify the genetic and neural changes underlying vocal divergence. Here we show that selection for song reshaped the canary song control system. Compared with breeds selected for plumage or body form, song breeds show increased neural progenitor proliferation and breed-specific changes in neuronal recruitment, sensorimotor brain region volume, and auditory sensitivity. Genome-wide analyses reveal a polygenic architecture underlying song divergence, enriched for transcriptional regulation and synaptic transmission genes. Among these, we find a coding variant in ADGRV1, the gene mutated in human Usher syndrome type 2C, associated with low-frequency singing and elevated auditory thresholds in canary. Disrupting ADGRV1 in zebrafish alters hair cell dynamics, linking adgrv1 mutation to a peripheral sensory mechanism. These findings demonstrate that learned vocal behavior can diversify rapidly through changes spanning sensory, neurogenic, and motor systems, with hearing itself as a substrate for selection.

evolutionary biology↗

bioRxiv2026

Extensive nuclear introgression accompanied ancient mitochondrial capture in the common ancestor of two sister hare species

Pleistocene climatic oscillations promoted contact and hybridization among hare species, leaving lasting genomic signatures. Two sister species, L. castroviejoi (broom hare, endemic to Iberia) and L. corsicanus (Italian hare, endemic to Italy), carry fixed mitogenomes from L. timidus (mountain hare), an Arctic species widespread in southern Europe before deglaciation. Whether such turnover was accompanied by nuclear introgression, and how it affects their genomes today, remains unclear. Here, we date the ancient mitochondrial replacement in the broom-Italian hare ancestor using whole mitogenomes incorporating Iron Age samples. Coalescent modelling of complete genomes infers a substantial mountain hare contribution (24%) to this ancestor ~900 Kya (~5N generations). Accordingly, phylogenetic segmentation identified genomic segments consistent with mountain-to-broom/Italian hare introgression, covering ~17.8% of the autosomes, close to ~18% expected under drift, given admixture's timing and magnitude. Genome polarisation corroborates this estimate, with 25-28% of the mountain hare genome polarising with broom and Italian hares rather than its sister Iberian hare, decreasing to 15-18% at diagnostic sites. The introgression segments concentrate fixed-introgression sites and show sharp transitions of ancestry at their borders. Highly introgressed regions are gene-dense, and regions of reduced introgression are repeat-rich, suggesting that recombination shapes the introgression landscape. They also harbour genes with mitochondrial function that mirror candidates linked to mito-nuclear coadaptation in the Iberian hare, hinting that mitonuclear interactions may influence which variants persist. Our study illustrates how combining demographic, phylogenomic and polarisation-based methods can quantify and localize extensive nuclear introgression, even in the absence of non-introgressed reference populations.

evolutionary biology↗

bioRxiv2026

Cryo-electron tomographic analysis of anti-nephrin-mediated podocytopathy

Nephrotic kidney diseases are characterized by proteinuria caused by dysfunction of the glomerular filtration barrier. Here, we perform an ultrastructural analysis of anti-nephrin-mediated podocytopathy by visualizing the near-native slit diaphragm in situ across defined stages of disease progression using cryo-electron tomography. Our analysis shows that at early disease stages punctuate cell-cell membrane approximations appear, with basal membrane apposition between adjacent podocyte foot processes, while the initially planar, fishnet slit diaphragm progressively bends into a dome-shaped configuration towards the urinary space. At later stages, slit diaphragm disappearance coincides with the appearance of endosomal and vesicular structures and extensive cytoskeletal reorganization. These cryo-electron tomography-based observations provide a structural framework for understanding how antibody binding to nephrin translates into podocyte architectural failure.

immunology↗

bioRxiv2026

Modulation of Avian Iridescence via Malanogenesis

The iridescent colors of birds originate in nanoscale feather structures that interact with light. Although the physical principles governing avian iridescence are well-established, the molecular mechanisms assembling these nanostructures into photonic materials remain unknown. Here, we integrated genomic, cellular, and optical approaches to investigate the molecular basis of iridescent color formation in birds. We leveraged mutations that arose in the domesticated Indian peafowl and natural color variation in wild birds. In peafowl, we identified eight genes underlying gains, losses, and shifts of iridescence, whereas in two wild species, we used single-cell transcriptomics to profile asymmetric feathers in which iridescent and non-iridescent barbules develop on opposite sides of the same feather. We found that all peafowl mutations mapped to melanogenesis genes, showing that variation in this pathway can modify diverse geometric features of feather photonic nanostructures. Mutations altering melanin composition collapsed multilayered photonic systems and yielded non-iridescent tissues, whereas changes in melanosome abundance, elongation, or deposition timing generated multilayer architectures with variable periodicity and color. We further show in peafowl that transitions from non-iridescent to iridescent plumage were associated with single-nucleotide mutations in a melanogenesis gene, suggesting that, in species already capable of forming multilayered nanostructures, iridescence can be gained by relatively small genetic changes. Single-cell transcriptomes from wild species also supported extensive melanocyte-centered regulatory rewiring associated with iridescence, including changes in melanosome maturation, trafficking, and intercellular signaling. Together, these results show that the nanoscale order underlying iridescence is developmentally plastic and highly responsive to the melanogenic environment. Significance StatementBird feathers can produce brilliant, shifting colors, but how these colors form during development has remained poorly understood. By comparing the genomes of color variants of domesticated peafowl and transcriptomes during feather development in wild birds, and combining these with chemical and optical analyses, we show that mutations in genes associated with melanogenesis can profoundly alter the amount, shape, and arrangement of the melanin granules inside feathers that interact with light and produce iridescence. These changes can switch feather appearance between dull and iridescent, or generate entirely new colors by restructuring how those granules are layered at the microscopic scale. Our results reveal a direct and flexible link between pigment production and the physical structures that generate iridescence in birds.

evolutionary biology↗

bioRxiv2025

Expansion, functional diversification and gene fusion events in the Ato protein family

Candida albicans, a commensal opportunistic pathogen, exhibits remarkable metabolic flexibility and adaptability to environmental changes. In glucose-limited niches, it utilizes alternative carbon sources such as carboxylic acids, which may influence its pathogenicity. In Saccharomyces cerevisiae, the uptake of monocarboxylates occurs through regulated plasma membrane (PM) transport proteins, such as Ato1 (Ady2), which belongs to the Acetate Uptake Transporter (AceTr) family. In C. albicans, these proteins are notably expanded, consisting of ten Ato-like proteins (ATO1-ATO10), whose functions remain unknown. Here, we investigated the role of Ato proteins in carboxylic acid utilization by C. albicans using in-silico and functional analysis. Our data revealed that several C. albicans Atos retain conserved AceTr motifs but possess distinct structural features, including differences in pore radius and binding sites for acetate and lactate. Expression analysis revealed that Ato1, Ato2, Ato3, and Ato6 exhibit distinct cellular localization and expression levels on the plasma membrane, depending on the presence or absence of monocarboxylates. Remarkably, deletion of ATO1 impaired Ato2 and Ato3 expression and caused ER retention of a distinct form of Ato2, suggesting a central regulatory role for Ato1 in the Ato transport system. Finally, we identified a novel Ato-related protein family in vertebrates. This family has three consecutive 6-helix transport domains and a unique C-terminal fusion with Sua5/YciO/YrdC, an enzyme involved in tRNA modification. Overall, our data suggests that the Ato protein family might play a critical role in the utilization of acetic or lactic acids in C. albicans. It also proposes potential functional redundancy among its members, which may contribute to rapid environmental adaptation and pathogenicity.

microbiology↗

bioRxiv2024

Bacterial metabolic remodelling by convergent evolution in response to host niche-dependent nutrient availability

New pathogens often arise after host jump events between species. However, our understanding of how bacterial pathogens pivot to distinct nutrient availabilities in a new host niche is limited. Staphylococcus aureus is a multi-host pathogen responsible for a global burden of disease in humans and farmed animals. Multiple human-to-bovine host switching events led to the emergence of S. aureus as a leading cause of intramammary infection in dairy cattle. Here, we employed ex vivo milk infections to investigate how bovine S. aureus has adapted to the dairy niche revealing metabolic remodelling including upregulation of genes for lactose utilisation and branched-chain amino acid biosynthesis in response to nutrient availability. Notably, infection of milk by bovine S. aureus results in a milk clotting phenotype associated with enhanced bacterial growth that is dependent on the protease aureolysin. The same adaptive phenotype has evolved convergently in different bovine S. aureus lineages via mutations in distinct regulatory gene loci that promote enhanced aureolysin expression. Taken together, we have dissected a key adaptive trait for a bacterial pathogen after a host-switch event, involving metabolic remodelling in response to the availability of nutrients. These findings highlight the remarkable evolutionary plasticity of S. aureus underpinning its multi-host species tropism.

microbiology↗

bioRxiv2024

Knowledge Innovation Ecosystem for the Promotion of User-Centre Health Innovations: Living Lab Methodology and Lessons Learned Through the Proposal of Standard Good Practices

Living Labs, experiencing a global surge in popularity over the past years, demands standardized guidance through the development of widely accepted good practices. While challenging due to the complex and evolving nature of Living Labs, this task remains essential. These knowledge innovation ecosystems facilitate a diverse array of interconnected and interacting end-users and stakeholder partners who engage collaboratively to co-create, embed, and/or leverage end-user-centric breakthroughs at one or more innovation phases within a real-world context. Based on the development of six Living Labs in the health domain, this study proposes a more general yet critical set of Living Labs good practices, emphasizing the importance of strong initial marketing and promotion strategies for Living Labs open calls, enforcing gender equality, carefully selecting stakeholders, devising and implementing effective framework strategies for end-user engagement and value creation, ensuring value creation for all Living Labs partners, prolonging the long-term viability of the Living Lab project, promoting and disseminating impactful actions and results, fostering environmental sustainability, and processing results data for Living Lab performance evaluation.

scientific communication and education↗

bioRxiv2023

Methylome-dependent transformation of emm1 group A streptococci

Genetic intractability presents a fundamental barrier to the manipulation of bacteria, hindering advancements in microbiological research. Group A Streptococcus (GAS), a lethal human pathogen currently associated with an unprecedented surge of infections world-wide, exhibits poor genetic tractability attributed to the activity of a conserved type 1 restriction modification system (RMS). RMS detect and cleave specific target sequences in foreign DNA that are protected in host DNA by sequence-specific methylation. Overcoming this "restriction barrier" thus presents a major technical challenge. Here we demonstrate for the first time that different RMS variants expressed by GAS give rise to genotype-specific and methylome-dependent variation in transformation efficiency. Further, we show that the magnitude of impact of methylation on transformation efficiency elicited by RMS variant TRDAG, encoded by all sequenced strains of the dominant and upsurge-associated emm1 genotype, is 100-fold greater than for all other TRD tested and is responsible for the poor transformation efficiency associated with this lineage. In dissecting the underlying mechanism, we developed an improved GAS transformation protocol whereby the restriction barrier is overcome by addition of the phage anti-restriction protein Ocr. This protocol is highly effective for TRDAG strains including clinical isolates representing all emm1 lineages, and will expedite critical research interrogating the genetics of emm1 GAS, negating the need to work in an RMS-negative background. These findings provide a striking example of the impact of RMS target sequence variation on bacterial transformation, and the importance of defining lineage-specific mechanisms of genetic recalcitrance. ImportanceUnderstanding the mechanisms by which bacterial pathogens are able to cause disease is essential to enable the targeted development of novel therapeutics. A key experimental approach to facilitate this research is the generation of bacterial mutants, through either specific gene deletions or sequence manipulation. This process relies on the ability to transform bacteria with exogenous DNA designed to generate the desired sequence changes. Bacteria have naturally developed protective mechanisms to detect and destroy invading DNA, and these systems severely impede the genetic manipulation of many important pathogens, including the lethal human pathogen group A Streptococcus (GAS). Many GAS lineages exist, of which emm1 is dominant among clinical isolates. Based on new experimental evidence, we identify the mechanism by which transformation is impaired in the emm1 lineage and establish an improved and highly efficient transformation protocol to expedite the generation of mutants.

microbiology↗

bioRxiv2022

Nanoscaled discovery of a shunt rifamycin from Salinispora arenicola using a three-colour GFP-tagged Staphylococcus aureus macrophage infection assay.

Antimicrobial resistance has emerged as an urgent global public health threat, and development of novel therapeutics for treating infections caused by multi-drug resistant bacteria is urgent. Staphylococcus aureus is a major human and animal pathogen, responsible for high levels of morbidity and mortality worldwide. The intracellular survival of S. aureus in macrophages contributes to immune evasion, dissemination, and resilience to antibiotic treatment. Here, we present a confocal fluorescence imaging assay for monitoring macrophage infection by GFP-tagged Staphylococcus aureus as a front-line tool to identify antibiotic leads. The assay was employed in combination with nanoscaled chemical analyses to facilitate the discovery of a novel, active rifamycin analogue. Our findings indicate a promising new approach to the identification of anti-microbial compounds with macrophage intracellular activity. The novel antibiotic identified here may represent a useful addition to our armoury in tackling the silent pandemic of antimicrobial resistance.

cell biology↗

bioRxiv2022

SIEVE: joint inference of single-nucleotide variants and cell phylogeny from single-cell DNA sequencing data

Single-cell DNA sequencing (scDNA-seq) has enabled the identification of single nucleotide somatic variants and the reconstruction of cell phylogenies. However, statistical phylogenetic models for cell phylogeny reconstruction from raw sequencing data are still in their infancy. Here we present SIEVE (SIngle-cell EVolution Explorer), a statistical method for the joint inference of somatic variants and cell phylogeny under the finite-sites assumption from scDNA-seq reads. SIEVE leverages raw read counts for all nucleotides at candidate variant sites, and corrects the acquisition bias of branch lengths. In our simulations, SIEVE outperforms other methods both in phylogenetic accuracy and variant calling accuracy. We apply SIEVE to three scDNA-seq datasets, for colorectal (CRC) and triple-negative breast cancer (TNBC), one of them generated by us. On simulated data, SIEVE reliably infers homo-and heterozygous somatic variants. The analysis of real data uncovers that double mutant genotypes are rare in CRC but unexpectedly frequent in TNBC samples.

bioinformatics↗

bioRxiv2021

Long non-coding RNA Neat1 is a key translational regulator in hypoxia.

Internal ribosome entry sites (IRESs) drive translation initiation during stress. In response to hypoxia, (lymph)angiogenic factors responsible for tissue revascularization in ischemic diseases are induced by the IRES-dependent mechanism. Here we searched for IRES trans-acting factors (ITAFs) active in early hypoxia in mouse cardiomyocytes. Using knock-down and proteomics approaches, we show a link between a stressed-induced nuclear body, the paraspeckle, and IRES-dependent translation. Furthermore, smiFISH experiments demonstrate the recruitment of IRES-containing mRNA into paraspeckle during hypoxia. Our data reveal that the long non-coding RNA Neat1, an essential paraspeckle component, is a key translational regulator, active on IRESs of (lymph)angiogenic and cardioprotective factor mRNAs. In addition, paraspeckle proteins p54nrb and PSPC1 as well as nucleolin and Rps2, two p54nrb-interacting proteins identified by mass spectrometry, are ITAFs for IRES subgroups. Paraspeckle thus appears as a platform to recruit IRES-containing mRNAs and possibly host IRESome assembly. Polysome PCR array shows that Neat1 isoforms regulate IRES-dependent translation and, more widely, translation of mRNAs involved in stress response. HighlightsO_LIParaspeckle formation correlates with activation of translation via internal ribosome entry sites (IRES) in mouse hypoxic cardiomyocytes as well as in tumoral cells. C_LIO_LIThe long non-coding RNA Neat1, an essential paraspeckle component, is a key translational regulator of (lymph)angiogenic and cardioprotective factor expression in this process. C_LIO_LIIRES-containing mRNA is recruited into paraspeckles during hypoxia. C_LIO_LIParaspeckle proteins p54nrb and PSPC1 as well as two p54nrb-interacting proteins, nucleolin and RPS2, contribute to this process. C_LIO_LIParaspeckle appears as a platform for IRESome formation in the nucleus. C_LIO_LIThe Neat1 isoforms widely regulate the translation of mRNAs containing IRESs and of genes involved in the stress response. C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/430272v2_ufig1.gif" ALT="Figure 1"> View larger version (98K): org.highwire.dtl.DTLVardef@1741648org.highwire.dtl.DTLVardef@62e741org.highwire.dtl.DTLVardef@13c86a8org.highwire.dtl.DTLVardef@acae63_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

bioRxiv2020

Population analysis of Legionella pneumophila reveals the basis of resistance to complement-mediated killing

Legionella pneumophila is the most common cause of the severe respiratory infection known as Legionnaires disease. L. pneumophila is typically a symbiont of free-living amoeba, and our understanding of the bacterial factors that determine human pathogenicity is limited. Here we carried out a population genomic study of 900 L. pneumophila isolates from human clinical and environmental samples to examine their genetic diversity, global distribution and the basis for human pathogenicity. We found that although some clones are more commonly associated with clinical infections, the capacity for human disease is representative of the breadth of species diversity. To investigate the bacterial genetic basis for human disease potential, we carried out a genome-wide association study that identified a single gene (lag-1), to be most strongly associated with clinical isolates. Molecular evolutionary analysis showed that lag-1, which encodes an O-acetyltransferase responsible for lipopolysaccharide modification, has been distributed horizontally across all major phylogenetic clades of L. pneumophila by frequent recent recombination events. Functional analysis revealed a correlation between the presence of a functional lag-1 gene and resistance to killing in human serum and bovine broncho-alveolar lavage. In addition, L. pneumophila strains that express lag-1 escaped complement-mediated phagocytosis by neutrophils. Importantly, we discovered that the expression of lag-1 confers the capacity to evade complement-mediated killing by inhibiting deposition of classical pathway molecules on the bacterial surface. In summary, our combined population and functional analyses identified L. pneumophila genetic traits linked to human disease and revealed the molecular basis for resistance to complement-mediated killing, a previously elusive trait of direct relevance to human disease pathogenicity. SignificanceLegionella pneumophila is an environmental bacterium associated with a severe pneumonia known as Legionnaires disease. A small number of L. pneumophila clones are responsible for a large proportion of human infections suggesting they have enhanced pathogenicity. Here, we employed a large-scale population analysis to investigate the evolution of human pathogenicity and identified a single gene (lag-1) that was more frequently found in clinical isolates. Functional analysis revealed that the lag-1-encoded O-acetyltransferase, involved in modification of lipopolysaccharide, conferred resistance to the classical pathway of complement in human serum. These findings solve a long-standing mystery in the field regarding L. pneumophila resistance to serum killing, revealing a novel mechanism by which L. pneumophila may avoid immune defences during infection.

microbiology↗

bioRxiv2019

NeuroPycon: A free Python toolbox for fast multi-modal and reproducible brain connectivity pipelines

Recent years have witnessed a massive push towards reproducible research in neuroscience. Unfortunately, this endeavor is often challenged by the large diversity of tools used, project-specific custom code and the difficulty to track all user-defined parameters. NeuroPycon is an open-source multi-modal brain data analysis toolkit which provides Python-based template pipelines for advanced multi-processing of MEG, EEG, functional and anatomical MRI data, with a focus on connectivity and graph theoretical analyses. Importantly, it provides shareable parameter files to facilitate replication of all analysis steps. NeuroPycon is based on the NiPype framework which facilitates data analyses by wrapping many commonly-used neuroimaging software tools into a common Python environment. In other words, rather than being a brain imaging software with is own implementation of standard algorithms for brain signal processing, NeuroPycon seamlessly integrates existing packages (coded in python, Matlab or other languages) into a unified python framework. Importantly, thanks to the multi-threaded processing and computational efficiency afforded by NiPype, NeuroPycon provides an easy option for fast parallel processing, which critical when handling large sets of multi-dimensional brain data. Moreover, its flexible design allows users to easily configure analysis pipelines by connecting distinct nodes to each other. Each node can be a Python-wrapped module, a user-defined function or a well-established tool (e.g. MNE-Python for MEG analysis, Radatools for graph theoretical metrics, etc.). Last but not least, the ability to use NeuroPycon parameter files to fully describe any pipeline is an important feature for reproducibility, as they can be shared and used for easy replication by others. The current implementation of NeuroPycon contains two complementary packages: The first, called ephypype, includes pipelines for electrophysiology analysis and a command-line interface for on the fly pipeline creation. Current implementations allow for MEG/EEG data import, pre-processing and cleaning by automatic removal of ocular and cardiac artefacts, in addition to sensor or source-level connectivity analyses. The second package, called graphpype, is designed to investigate functional connectivity via a wide range of graph-theoretical metrics, including modular partitions. The present article describes the philosophy, architecture, and functionalities of the toolkit and provides illustrative examples through interactive notebooks. NeuroPycon is available for download via github (https://github.com/neuropycon) and the two principal packages are documented online (https://neuropycon.github.io/ephypype/index.html. and https://neuropycon.github.io/graphpype/index.html). Future developments include fusion of multi-modal data (eg. MEG and fMRI or intracranial EEG and fMRI). We hope that the release of NeuroPycon will attract many users and new contributors, and facilitate the efforts of our community towards open source tool sharing and development, as well as scientific reproducibility.

neuroscience↗

bioRxiv2019

Chlamydia trachomatis outbreak: when the virulence-associated genome backbone imports a prevalence-associated major antigen signature

Chlamydia trachomatis is the most prevalent sexually transmitted bacteria worldwide and the causative agent of blinding trachoma. Strains are classified based on ompA genotypes, which are strongly linked with differential tissue tropism and disease outcomes. A lymphogranuloma venereum (LGV) epidemics, characterized by ulcerative proctitis, has emerged in the last two decades (mainly L2b genotype), raising high concern especially due to its circulation among men who have sex with men (MSM). Here, we report an ongoing outbreak (mostly affecting HIV-positive MSM engaging in high-risk practices) caused by an L2b strain with a rather unique genome makeup that precluded the laboratory notification of this outbreak as LGV due to its non-LGV ompA signature. Homologous recombination mediated the transfer of a ~4.5Kbp fragment enrolling CT681/ompA and neighboring genes (CT677/rrf, CT678/pyrH, CT679/tsf, CT680/rpsB) from a serovar D/Da strain likely possessing the typical T1 clade genome backbone associated with most prevalent genotypes (E and F). The hybrid L2b/D-Da strain presents the adhesin and immunodominant antigen MOMP (coded by ompA) with an epitope repertoire typical of non-invasive genital strains, while keeping the genome-dispersed virulence fingerprint of a classical LGV (L2b) strain. As previously reported for inter-clade ompA exchange among non-LGV clades, this unprecedented C. trachomatis genomic mosaic involving a contemporary epidemiologically and clinically relevant LGV strain may have implications on its transmission, tissue tropism and pathogenic capabilities. The emergence of such variants with epidemic and pathogenic potential highlights the need of more oriented surveillance strategies focused on capturing the C. trachomatis evolution in action.

genomics↗

bioRxiv2019

The dopamine receptor D5 gene shows signs of independent erosion in Toothed and Baleen whales

To compare gene loci considering a phylogenetic framework is a promising approach to uncover the genetic basis of human diseases. Imbalance of dopaminergic systems is suspected to underlie some emerging neurological disorders. The physiological functions of dopamine are transduced via G-protein-coupled receptors, including DRD5 which displays a relatively higher affinity towards dopamine. Importantly, DRD5 knockout mice are hypertense, a condition emerging from an increase in sympathetic tone. We investigated the evolution of DRD5, a high affinity receptor for dopamine, in mammals. Surprisingly, among 124 investigated mammalian genomes, we found that Cetacea lineages (Mysticeti and Odontoceti) have independently lost this gene, as well as the burrowing Chrysochloris asiatica (Cape golden mole). We suggest that DRD5 inactivation parallels hypoxia-induced adaptations, such as peripheral vasoconstriction required for deep-diving in Cetacea, in accordance with the convergent evolution of vasoconstrictor genes in hypoxia-exposed animals. Our findings indicate that Cetacea are natural knockouts for DRD5 and might offer valuable insights into the mechanisms of some forms of vasoconstriction responses and hypertension in humans.

evolutionary biology↗