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1. Toxin-like neuropeptides in the sea anemone Nematostella unravel recruitment from the nervous system to venom

   https://doi.org/10.1073/pnas.2011120117  

   Sachkova, Maria Y. ; Landau, Morani ; Surm, Joachim M. ; Macrander, Jason ; Singer, Shir A. ; Reitzel, Adam M. ; Moran, Yehu ( October 2020 , Proceedings of the National Academy of Sciences)

   The sea anemoneNematostella vectensis(Anthozoa, Cnidaria) is a powerful model for characterizing the evolution of genes functioning in venom and nervous systems. Although venom has evolved independently numerous times in animals, the evolutionary origin of many toxins remains unknown. In this work, we pinpoint an ancestral gene giving rise to a new toxin and functionally characterize both genes in the same species. Thus, we report a case of protein recruitment from the cnidarian nervous to venom system. The ShK-like1 peptide has a ShKT cysteine motif, is lethal for fish larvae and packaged into nematocysts, the cnidarian venom-producing stinging capsules. Thus, ShK-like1 is a toxic venom component. Its paralog, ShK-like2, is a neuropeptide localized to neurons and is involved in development. Both peptides exhibit similarities in their functional activities: They provoke contraction inNematostellapolyps and are toxic to fish. Because ShK-like2 but not ShK-like1 is conserved throughout sea anemone phylogeny, we conclude that the two paralogs originated due to aNematostella-specific duplication of a ShK-like2 ancestor, a neuropeptide-encoding gene, followed by diversification and partial functional specialization. ShK-like2 is represented by two gene isoforms controlled by alternative promoters conferring regulatory flexibility throughout development. Additionally, we characterized the expression patterns of four other peptides with structuralmore »similarities to studied venom components and revealed their unexpected neuronal localization. Thus, we employed genomics, transcriptomics, and functional approaches to reveal one venom component, five neuropeptides with two different cysteine motifs, and an evolutionary pathway from nervous to venom system in Cnidaria.

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2. VARIATION IN CONTRIBUTIONS OF ASEXUAL REPRODUCTION TO THE GENETIC STRUCTURE OF POPULATIONS OF THE SEA ANEMONE METRIDIUM SENILE

   https://doi.org/10.1111/j.1558-5646.1986.tb00477.x  

   Hoffmann, Richard J. ( March 1986 , Evolution)
3. The genome of Aiptasia , a sea anemone model for coral symbiosis

   https://doi.org/10.1073/pnas.1513318112  

   Baumgarten, Sebastian ; Simakov, Oleg ; Esherick, Lisl Y. ; Liew, Yi Jin ; Lehnert, Erik M. ; Michell, Craig T. ; Li, Yong ; Hambleton, Elizabeth A. ; Guse, Annika ; Oates, Matt E. ; et al ( September 2015 , Proceedings of the National Academy of Sciences)
4. The mitochondrial genome of a sea anemone Bolocera sp. exhibits novel genetic structures potentially involved in adaptation to the deep-sea environment

   https://doi.org/10.1002/ece3.3067  

   Zhang, Bo ; Zhang, Yan-Hong ; Wang, Xin ; Zhang, Hui-Xian ; Lin, Qiang ( July 2017 , Ecology and Evolution)
5. A novel regulatory gene promotes novel cell fate by suppressing ancestral fate in the sea anemone Nematostella vectensis

   https://doi.org/10.1073/pnas.2113701119  

   Babonis, Leslie S. ; Enjolras, Camille ; Ryan, Joseph F. ; Martindale, Mark Q. ( May 2022 , Proceedings of the National Academy of Sciences)

   Cnidocytes (i.e., stinging cells) are an unequivocally novel cell type used by cnidarians (i.e., corals, jellyfish, and their kin) to immobilize prey. Although they are known to share a common evolutionary origin with neurons, the developmental program that promoted the emergence of cnidocyte fate is not known. Using functional genomics in the sea anemone, Nematostella vectensis , we show that cnidocytes develop by suppression of neural fate in a subset of neurons expressing RFamide. We further show that a single regulatory gene, a C 2 H 2 -type zinc finger transcription factor (ZNF845), coordinates both the gain of novel (cnidocyte-specific) traits and the inhibition of ancestral (neural) traits during cnidocyte development and that this gene arose by domain shuffling in the stem cnidarian. Thus, we report a mechanism by which a truly novel regulatory gene (ZNF845) promotes the development of a truly novel cell type (cnidocyte) through duplication of an ancestral cell lineage (neuron) and inhibition of its ancestral identity (RFamide).