The Tiger Rattlesnake genome reveals a complex genotype underlying a simple venom phenotype.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
26 01 2021
Historique:
entrez: 20 1 2021
pubmed: 21 1 2021
medline: 12 6 2021
Statut: ppublish

Résumé

Variation in gene regulation is ubiquitous, yet identifying the mechanisms producing such variation, especially for complex traits, is challenging. Snake venoms provide a model system for studying the phenotypic impacts of regulatory variation in complex traits because of their genetic tractability. Here, we sequence the genome of the Tiger Rattlesnake, which possesses the simplest and most toxic venom of any rattlesnake species, to determine whether the simple venom phenotype is the result of a simple genotype through gene loss or a complex genotype mediated through regulatory mechanisms. We generate the most contiguous snake-genome assembly to date and use this genome to show that gene loss, chromatin accessibility, and methylation levels all contribute to the production of the simplest, most toxic rattlesnake venom. We provide the most complete characterization of the venom gene-regulatory network to date and identify key mechanisms mediating phenotypic variation across a polygenic regulatory network.

Identifiants

pubmed: 33468678
pii: 2014634118
doi: 10.1073/pnas.2014634118
pmc: PMC7848695
pii:
doi:

Substances chimiques

Crotalid Venoms 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIGMS NIH HHS
ID : P20 GM109094
Pays : United States
Organisme : NHGRI NIH HHS
ID : R21 HG010403
Pays : United States

Déclaration de conflit d'intérêts

The authors declare no competing interest.

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Auteurs

Mark J Margres (MJ)

Department of Biological Sciences, Clemson University, Clemson, SC 29634; margres@usf.edu viper@clemson.edu.
Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138.
Department of Integrative Biology, University of South Florida, Tampa, FL 33620.

Rhett M Rautsaw (RM)

Department of Biological Sciences, Clemson University, Clemson, SC 29634.

Jason L Strickland (JL)

Department of Biological Sciences, Clemson University, Clemson, SC 29634.
Department of Biology, University of South Alabama, Mobile, AL 36688.

Andrew J Mason (AJ)

Department of Biological Sciences, Clemson University, Clemson, SC 29634.

Tristan D Schramer (TD)

Department of Biological Sciences, Clemson University, Clemson, SC 29634.

Erich P Hofmann (EP)

Department of Biological Sciences, Clemson University, Clemson, SC 29634.

Erin Stiers (E)

Department of Biological Sciences, Clemson University, Clemson, SC 29634.

Schyler A Ellsworth (SA)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Gunnar S Nystrom (GS)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Michael P Hogan (MP)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Daniel A Bartlett (DA)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Timothy J Colston (TJ)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

David M Gilbert (DM)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Darin R Rokyta (DR)

Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Christopher L Parkinson (CL)

Department of Biological Sciences, Clemson University, Clemson, SC 29634; margres@usf.edu viper@clemson.edu.
Department of Forestry and Environmental Conservation, Clemson University, Clemson, SC 29634.

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