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Lindblad-Toh, KerstinORCID iD iconorcid.org/0000-0001-8338-0253
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Publications (10 of 157) Show all publications
Mataix-Cols, D., Hansen, B., Mattheisen, M., Karlsson, E. K., Addington, A. M., Boberg, J., . . . Crowley, J. J. (2020). Nordic OCD & Related Disorders Consortium: Rationale, design, and methods.. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 183(1), 38-50
Open this publication in new window or tab >>Nordic OCD & Related Disorders Consortium: Rationale, design, and methods.
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2020 (English)In: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, ISSN 1552-4841, E-ISSN 1552-485X, Vol. 183, no 1, p. 38-50Article in journal (Refereed) Published
Abstract [en]

Obsessive-compulsive disorder (OCD) is a debilitating psychiatric disorder, yet its etiology is unknown and treatment outcomes could be improved if biological targets could be identified. Unfortunately, genetic findings for OCD are lagging behind other psychiatric disorders. Thus, there is a pressing need to understand the causal mechanisms implicated in OCD in order to improve clinical outcomes and to reduce morbidity and societal costs. Specifically, there is a need for a large-scale, etiologically informative genetic study integrating genetic and environmental factors that presumably interact to cause the condition. The Nordic countries provide fertile ground for such a study, given their detailed population registers, national healthcare systems and active specialist clinics for OCD. We thus formed the Nordic OCD and Related Disorders Consortium (NORDiC, www.crowleylab.org/nordic), and with the support of NIMH and the Swedish Research Council, have begun to collect a large, richly phenotyped and genotyped sample of OCD cases. Our specific aims are geared toward answering a number of key questions regarding the biology, etiology, and treatment of OCD. This article describes and discusses the rationale, design, and methodology of NORDiC, including details on clinical measures and planned genomic analyses.

Keywords
Denmark, GWAS, Norway, OCD, Sweden, genetic
National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-401535 (URN)10.1002/ajmg.b.32756 (DOI)31424634 (PubMedID)
Available from: 2020-01-08 Created: 2020-01-08 Last updated: 2020-02-05Bibliographically approved
Chen, J., Swofford, R., Johnson, J., Cummings, B. B., Rogel, N., Lindblad-Toh, K., . . . Regev, A. (2019). A quantitative framework for characterizing the evolutionary history of mammalian gene expression. Genome Research, 29(1), 53-63
Open this publication in new window or tab >>A quantitative framework for characterizing the evolutionary history of mammalian gene expression
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2019 (English)In: Genome Research, ISSN 1088-9051, E-ISSN 1549-5469, Vol. 29, no 1, p. 53-63Article in journal (Refereed) Published
Abstract [en]

The evolutionary history of a gene helps predict its function and relationship to phenotypic traits. Although sequence conservation is commonly used to decipher gene function and assess medical relevance, methods for functional inference from comparative expression data are lacking. Here, we use RNA-seq across seven tissues from 17 mammalian species to show that expression evolution across mammals is accurately modeled by the Ornstein-Uhlenbeck process, a commonly proposed model of continuous trait evolution. We apply this model to identify expression pathways under neutral, stabilizing, and directional selection. We further demonstrate novel applications of this model to quantify the extent of stabilizing selection on a gene's expression, parameterize the distribution of each gene's optimal expression level, and detect deleterious expression levels in expression data from individual patients. Our work provides a statistical framework for interpreting expression data across species and in disease.

National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-374111 (URN)10.1101/gr.237636.118 (DOI)000454707900005 ()30552105 (PubMedID)
Funder
Swedish Research Council
Available from: 2019-01-23 Created: 2019-01-23 Last updated: 2019-01-23Bibliographically approved
Farias, F. H. G., Dahlqvist, J., Kozyrev, S. V., Leonard, D., Wilbe, M., Abramov, S., . . . Lindblad-Toh, K. (2019). A rare regulatory variant in the MEF2D gene affects gene regulation and splicing and is associated with a SLE sub-phenotype in Swedish cohorts. European Journal of Human Genetics, 27, 432-441
Open this publication in new window or tab >>A rare regulatory variant in the MEF2D gene affects gene regulation and splicing and is associated with a SLE sub-phenotype in Swedish cohorts
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2019 (English)In: European Journal of Human Genetics, ISSN 1018-4813, E-ISSN 1476-5438, Vol. 27, p. 432-441Article in journal (Refereed) Published
Abstract [en]

Systemic lupus erythematosus (SLE) is an autoimmune disorder with heterogeneous clinical presentation and complex etiology involving the interplay between genetic, epigenetic, environmental and hormonal factors. Many common SNPs identified by genome wide-association studies (GWAS) explain only a small part of the disease heritability suggesting the contribution from rare genetic variants, undetectable in GWAS, and complex epistatic interactions. Using targeted re-sequencing of coding and conserved regulatory regions within and around 215 candidate genes selected on the basis of their known role in autoimmunity and genes associated with canine immune-mediated diseases, we identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1-10). Fisher's exact test revealed an association between the genetic variant and a triad of disease manifestations including Raynaud, anti-U1-ribonucleoprotein (anti-RNP), and anti-Smith (anti-Sm) antibodies (p = 0.00037) among the patients. The DNA-binding activity of the allele was further studied by EMSA, reporter assays, and minigenes. The region has properties of an active cell-specific enhancer, differentially affected by the alleles of rs200395694:G > T. In addition, the risk allele exerts an inhibitory effect on the splicing of the alternative tissue-specific isoform, and thus may modify the target gene set regulated by this isoform. These findings emphasize the potential of dissecting traits of complex diseases and correlating them with rare risk alleles with strong biological effects.

National Category
Medical Genetics
Research subject
Medical Science
Identifiers
urn:nbn:se:uu:diva-368313 (URN)10.1038/s41431-018-0297-x (DOI)000458626500013 ()30459414 (PubMedID)
Funder
Swedish Research CouncilSwedish Research Council FormasSwedish Rheumatism AssociationKnut and Alice Wallenberg Foundation
Note

These authors contributed equally: Johanna Dahlqvist, Sergey V. Kozyrev, Dag Leonard, Maria Wilbe

Available from: 2018-12-04 Created: 2018-12-04 Last updated: 2019-03-11Bibliographically approved
Biasoli, D., Compston-Garnett, L., Ricketts, S. L., Birand, Z., Courtay-Cahen, C., Fineberg, E., . . . Starkey, M. (2019). A synonymous germline variant in a gene encoding a cell adhesion molecule is associated with cutaneous mast cell tumour development in Labrador and Golden Retrievers. PLoS Genetics, 15(3), Article ID e1007967.
Open this publication in new window or tab >>A synonymous germline variant in a gene encoding a cell adhesion molecule is associated with cutaneous mast cell tumour development in Labrador and Golden Retrievers
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2019 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 15, no 3, article id e1007967Article in journal (Refereed) Published
Abstract [en]

Mast cell tumours are the most common type of skin cancer in dogs, representing a significant concern in canine health. The molecular pathogenesis is largely unknown, but breed-predisposition for mast cell tumour development suggests the involvement of inherited genetic risk factors in some breeds. In this study, we aimed to identify germline risk factors associated with the development of mast cell tumours in Labrador Retrievers, a breed with an elevated risk of mast cell tumour development. Using a methodological approach that combined a genome-wide association study, targeted next generation sequencing, and TaqMan genotyping, we identified a synonymous variant in the DSCAM gene on canine chromosome 31 that is associated with mast cell tumours in Labrador Retrievers. DSCAM encodes a cell-adhesion molecule. We showed that the variant has no effect on the DSCAM mRNA level but is associated with a significant reduction in the level of the DSCAM protein, suggesting that the variant affects the dynamics of DSCAM mRNA translation. Furthermore, we showed that the variant is also associated with mast cell tumours in Golden Retrievers, a breed that is closely related to Labrador Retrievers and that also has a predilection for mast cell tumour development. The variant is common in both Labradors and Golden Retrievers and consequently is likely to be a significant genetic contributor to the increased susceptibility of both breeds to develop mast cell tumours. The results presented here not only represent an important contribution to the understanding of mast cell tumour development in dogs, as they highlight the role of cell adhesion in mast cell tumour tumourigenesis, but they also emphasise the potential importance of the effects of synonymous variants in complex diseases such as cancer. Author summary The combination of various genetic and environmental risk factors makes the understanding of the molecular circuitry behind complex diseases, like cancer, a major challenge. The homogeneous nature of pedigree dog breed genomes makes these dogs ideal for the identification of both simple disease-causing genetic variants and genetic risk factors for complex diseases. Mast cell tumours are the most common type of canine skin cancer, and one of the most common cancers affecting dogs of most breeds. Several breeds, including Labrador Retrievers (which represent one of the most popular dog breeds), have an elevated risk of mast cell tumour development. Here, by using a methodological approach that combined different techniques, we identified a common inherited synonymous variant, that predisposes Labrador Retrievers to mast cell tumour development. Interestingly, we showed that this variant, despite its synonymous nature, appears to have an effect on translation dynamics as it is associated with reduced levels of DSCAM, a cell adhesion molecule. The results presented here reveal dysregulation of cell adhesion to be an important factor in mast cell tumour pathogenesis, and also highlight the important role that synonymous variants can play in complex diseases.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2019
National Category
Immunology
Identifiers
urn:nbn:se:uu:diva-382472 (URN)10.1371/journal.pgen.1007967 (DOI)000462994900012 ()30901340 (PubMedID)
Available from: 2019-05-02 Created: 2019-05-02 Last updated: 2019-05-02Bibliographically approved
Beichman, A. C., Koepfli, K.-P., Li, G., Murphy, W., Dobrynin, P., Kliver, S., . . . Wayne, R. K. (2019). Aquatic Adaptation and Depleted Diversity: A Deep Dive into the Genomes of the Sea Otter and Giant Otter.. Molecular biology and evolution, 36(12), 2631-2655
Open this publication in new window or tab >>Aquatic Adaptation and Depleted Diversity: A Deep Dive into the Genomes of the Sea Otter and Giant Otter.
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2019 (English)In: Molecular biology and evolution, ISSN 0737-4038, E-ISSN 1537-1719, Vol. 36, no 12, p. 2631-2655Article in journal (Refereed) Published
Abstract [en]

Despite its recent invasion into the marine realm, the sea otter (Enhydra lutris) has evolved a suite of adaptations for life in cold coastal waters, including limb modifications and dense insulating fur. This uniquely dense coat led to the near-extinction of sea otters during the 18th-20th century fur trade and an extreme population bottleneck. We used the de novo genome of the southern sea otter (E. l. nereis) to reconstruct its evolutionary history, identify genes influencing aquatic adaptation, and detect signals of population bottlenecks. We compared the genome of the southern sea otter with the tropical freshwater-living giant otter (Pteronura brasiliensis) to assess common and divergent genomic trends between otter species, and with the closely related northern sea otter (E. l. kenyoni) to uncover population-level trends. We found signals of positive selection in genes related to aquatic adaptations, particularly limb development and polygenic selection on genes related to hair follicle development. We found extensive pseudogenization of olfactory receptor genes in both the sea otter and giant otter lineages, consistent with patterns of sensory gene loss in other aquatic mammals. At the population level, the southern sea otter and the northern sea otter showed extremely low genomic diversity, signals of recent inbreeding, and demographic histories marked by population declines. These declines may predate the fur trade and appear to have resulted in an increase in putatively deleterious variants that could impact the future recovery of the sea otter.

Keywords
adaptation, deleterious variation, demography, genomics, giant otter, olfaction, population genetics, pseudogenes, sea otter
National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-401536 (URN)10.1093/molbev/msz101 (DOI)000501735000001 ()31212313 (PubMedID)
Available from: 2020-01-08 Created: 2020-01-08 Last updated: 2020-01-13Bibliographically approved
Megquier, K., Genereux, D. P., Hekman, J., Swofford, R., Turner-Maier, J., Johnson, J., . . . Karlsson, E. K. (2019). BarkBase: Epigenomic Annotation of Canine Genomes. Genes, 10(6), Article ID 433.
Open this publication in new window or tab >>BarkBase: Epigenomic Annotation of Canine Genomes
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2019 (English)In: Genes, ISSN 2073-4425, E-ISSN 2073-4425, Vol. 10, no 6, article id 433Article in journal (Refereed) Published
Abstract [en]

Dogs are an unparalleled natural model for investigating the genetics of health and disease, particularly for complex diseases like cancer. Comprehensive genomic annotation of regulatory elements active in healthy canine tissues is crucial both for identifying candidate causal variants and for designing functional studies needed to translate genetic associations into disease insight. Currently, canine geneticists rely primarily on annotations of the human or mouse genome that have been remapped to dog, an approach that misses dog-specific features. Here, we describe BarkBase, a canine epigenomic resource available at barkbase.org. BarkBase hosts data for 27 adult tissue types, with biological replicates, and for one sample of up to five tissues sampled at each of four carefully staged embryonic time points. RNA sequencing is complemented with whole genome sequencing and with assay for transposase-accessible chromatin using sequencing (ATAC-seq), which identifies open chromatin regions. By including replicates, we can more confidently discern tissue-specific transcripts and assess differential gene expression between tissues and timepoints. By offering data in easy-to-use file formats, through a visual browser modeled on similar genomic resources for human, BarkBase introduces a powerful new resource to support comparative studies in dogs and humans.

Place, publisher, year, edition, pages
MDPI, 2019
Keywords
dog, expression, genome, annotation, ATAC-seq, RNA-seq, epigenomic, canine, comparative
National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-390646 (URN)10.3390/genes10060433 (DOI)000473797000028 ()31181663 (PubMedID)
Funder
NIH (National Institute of Health), 5R24OD018250
Available from: 2019-08-19 Created: 2019-08-19 Last updated: 2019-08-19Bibliographically approved
Megquier, K., Turner-Maier, J., Swofford, R., Kim, J.-H., Sarver, A. L., Wang, C., . . . Lindblad-Toh, K. (2019). Comparative Genomics Reveals Shared Mutational Landscape in Canine Hemangiosarcoma and Human Angiosarcoma. Molecular Cancer Research, 17(12), 2410-2421
Open this publication in new window or tab >>Comparative Genomics Reveals Shared Mutational Landscape in Canine Hemangiosarcoma and Human Angiosarcoma
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2019 (English)In: Molecular Cancer Research, ISSN 1541-7786, E-ISSN 1557-3125, Vol. 17, no 12, p. 2410-2421Article in journal (Refereed) Published
Abstract [en]

Angiosarcoma is a highly aggressive cancer of blood vessel-forming cells with few effective treatment options and high patient mortality. It is both rare and heterogenous, making large, well-powered genomic studies nearly impossible. Dogs commonly suffer from a similar cancer, called hemangiosarcoma, with breeds like the golden retriever carrying heritable genetic factors that put them at high risk. If the clinical similarity of canine hemangiosarcoma and human angiosarcoma reflects shared genomic etiology, dogs could be a critically needed model for advancing angiosarcoma research. We assessed the genomic landscape of canine hemangiosarcoma via whole-exome sequencing (47 golden retriever hemangiosarcomas) and RNA sequencing (74 hemangiosarcomas from multiple breeds). Somatic coding mutations occurred most frequently in the tumor suppressor TP53 (59.6% of cases) as well as two genes in the PI3K pathway: the oncogene PIK3CA (29.8%) and its regulatory subunit PIK3R1 (8.5%). The predominant mutational signature was the age-associated deamination of cytosine to thymine. As reported in human angiosarcoma, CDKN2A/B was recurrently deleted and VEGFA, KDR, and KIT recurrently gained. We compared the canine data to human data recently released by The Angiosarcoma Project, and found many of the same genes and pathways significantly enriched for somatic mutations, particularly in breast and visceral angiosarcomas. Canine hemangiosarcoma closely models the genomic landscape of human angiosarcoma of the breast and viscera, and is a powerful tool for investigating the pathogenesis of this devastating disease. IMPLICATIONS: We characterize the genomic landscape of canine hemangiosarcoma and demonstrate its similarity to human angiosarcoma.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-399825 (URN)10.1158/1541-7786.MCR-19-0221 (DOI)000500951800006 ()31570656 (PubMedID)
Funder
Swedish Cancer SocietySwedish Research Council
Available from: 2019-12-16 Created: 2019-12-16 Last updated: 2020-01-13Bibliographically approved
Hitte, C., Le Beguec, C., Cadieu, E., Wucher, V., Primot, A., Prouteau, P., . . . Derrien, T. (2019). Genome-Wide Analysis of Long Non-Coding RNA Profiles in Canine Oral Melanomas. Genes, 10(6), Article ID 477.
Open this publication in new window or tab >>Genome-Wide Analysis of Long Non-Coding RNA Profiles in Canine Oral Melanomas
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2019 (English)In: Genes, ISSN 2073-4425, E-ISSN 2073-4425, Vol. 10, no 6, article id 477Article in journal (Refereed) Published
Abstract [en]

Mucosal melanomas (MM) are rare aggressive cancers in humans, and one of the most common forms of oral cancers in dogs. Similar biological and histological features are shared between MM in both species, making dogs a powerful model for comparative oncology studies of melanomas. Although exome sequencing recently identified recurrent coding mutations in canine MM, little is known about changes in non-coding gene expression, and more particularly, in canine long non-coding RNAs (lncRNAs), which are commonly dysregulated in human cancers. Here, we sampled a large cohort (n = 52) of canine normal/tumor oral MM from three predisposed breeds (poodles, Labrador retrievers, and golden retrievers), and used deep transcriptome sequencing to identify more than 400 differentially expressed (DE) lncRNAs. We further prioritized candidate lncRNAs by comparative genomic analysis to pinpoint 26 dog-human conserved DE lncRNAs, including SOX21-AS, ZEB2-AS, and CASC15 lncRNAs. Using unsupervised co-expression network analysis with coding genes, we inferred the potential functions of the DE lncRNAs, suggesting associations with cancer-related genes, cell cycle, and carbohydrate metabolism Gene Ontology (GO) terms. Finally, we exploited our multi-breed design to identify DE lncRNAs within breeds. This study provides a unique transcriptomic resource for studying oral melanoma in dogs, and highlights lncRNAs that may potentially be diagnostic or therapeutic targets for human and veterinary medicine.

Place, publisher, year, edition, pages
MDPI, 2019
Keywords
mucosal melanoma, dogs, transcriptome sequencing, long non-coding RNAs (lncRNAs)
National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-390645 (URN)10.3390/genes10060477 (DOI)000473797000072 ()31234577 (PubMedID)
Available from: 2019-08-19 Created: 2019-08-19 Last updated: 2019-08-19Bibliographically approved
Hindle, A. G., Allen, K. N., Batten, A. J., Huckastadt, L. A., Turner-Maier, J., Schulberg, S. A., . . . Buys, E. S. (2019). Low guanylyl cyclase activity in Weddell seals: implications for peripheral vasoconstriction and perfusion of the brain during diving. American Journal of Physiology. Regulatory Integrative and Comparative Physiology, 316(6), R704-R715
Open this publication in new window or tab >>Low guanylyl cyclase activity in Weddell seals: implications for peripheral vasoconstriction and perfusion of the brain during diving
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2019 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 316, no 6, p. R704-R715Article in journal (Refereed) Published
Abstract [en]

Nitric oxide (NO) is a potent vasodilator, which improves perfusion and oxygen delivery during tissue hypoxia in terrestrial animals. The vertebrate dive response involves vasoconstriction in select tissues. which persists despite profound hypoxia. Using tissues collected from Weddell seals at necropsy, we investigated whether vasoconstriction is aided by downregulation of local hypoxia signaling mechanisms. We focused on NO-soluble guanylyl cyclasc (GC)-cGMP signaling, a well-known vasodilatory transduction pathway. Seals have a lower GC protein abundance. activity, and capacity to respond to NO stimulation than do terrestrial mammals. In seal lung homogenates, GC produced less cGMP (20.1 +/- 3.7 pmol.mg protein(-1).min(-1)) than the lungs of dogs (-80 +/- 144 pmol.mg protein(-1).min(-1) less than seals), sheep (-472 +/- 96), rats (-664 +/- 104) or mice ( -1,160 +/- 104, P < 0.0001). Amino acid sequences of the GC enzyme alpha-subunits differed between seals and terrestrial mammals, potentially affecting their structure and function. Vasoconstriction in diving Weddell seals is not consistent across tissues; perfusion is maintained in the brain and heart but decreased in other organs such as the kidney. A NO donor increased median GC activity 49.5-fold in the seal brain but only 27.4-fold in the kidney. consistent with the priority of cerebral perfusion during diving. Nos3 expression was high in the seal brain, which could improve NO production and vasodilatory potential. Conversely, Pde5a expression was high in the seal renal artery, which may increase cGMP breakdown and vasoconstriction in the kidney. Taken together, the results of this study suggest that alterations in the NO-cGMP pathway facilitate the diving response.

Place, publisher, year, edition, pages
AMER PHYSIOLOGICAL SOC, 2019
Keywords
dive response, NO-cGMP signaling, pinniped, soluble guanylate cyclase
National Category
Physiology
Identifiers
urn:nbn:se:uu:diva-386431 (URN)10.1152/ajpregu.00283.2018 (DOI)000469020400002 ()30892912 (PubMedID)
Available from: 2019-06-26 Created: 2019-06-26 Last updated: 2019-06-26Bibliographically approved
Casewell, N. R., Petras, D., Card, D. C., Suranse, V., Mychajliw, A. M., Richards, D., . . . Turvey, S. T. (2019). Solenodon genome reveals convergent evolution of venom in eulipotyphlan mammals.. Proceedings of the National Academy of Sciences of the United States of America, 116(51), 25745-25755
Open this publication in new window or tab >>Solenodon genome reveals convergent evolution of venom in eulipotyphlan mammals.
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2019 (English)In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 116, no 51, p. 25745-25755Article in journal (Refereed) Published
Abstract [en]

Venom systems are key adaptations that have evolved throughout the tree of life and typically facilitate predation or defense. Despite venoms being model systems for studying a variety of evolutionary and physiological processes, many taxonomic groups remain understudied, including venomous mammals. Within the order Eulipotyphla, multiple shrew species and solenodons have oral venom systems. Despite morphological variation of their delivery systems, it remains unclear whether venom represents the ancestral state in this group or is the result of multiple independent origins. We investigated the origin and evolution of venom in eulipotyphlans by characterizing the venom system of the endangered Hispaniolan solenodon (Solenodon paradoxus). We constructed a genome to underpin proteomic identifications of solenodon venom toxins, before undertaking evolutionary analyses of those constituents, and functional assessments of the secreted venom. Our findings show that solenodon venom consists of multiple paralogous kallikrein 1 (KLK1) serine proteases, which cause hypotensive effects in vivo, and seem likely to have evolved to facilitate vertebrate prey capture. Comparative analyses provide convincing evidence that the oral venom systems of solenodons and shrews have evolved convergently, with the 4 independent origins of venom in eulipotyphlans outnumbering all other venom origins in mammals. We find that KLK1s have been independently coopted into the venom of shrews and solenodons following their divergence during the late Cretaceous, suggesting that evolutionary constraints may be acting on these genes. Consequently, our findings represent a striking example of convergent molecular evolution and demonstrate that distinct structural backgrounds can yield equivalent functions.

Keywords
convergent molecular evolution, gene duplication, genotype phenotype, kallikrein toxin, venom systems
National Category
Evolutionary Biology
Identifiers
urn:nbn:se:uu:diva-401532 (URN)10.1073/pnas.1906117116 (DOI)000503281500058 ()31772017 (PubMedID)
Funder
Wellcome trust, 200517/Z/16/ZSwedish Research CouncilAustralian Research Council, DE160101142German Research Foundation (DFG), PE 2600/1
Available from: 2020-01-08 Created: 2020-01-08 Last updated: 2020-01-22Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0001-8338-0253

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