| Autor: |
Babonis LS; Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, FL 32080., Enjolras C; Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, FL 32080., Ryan JF; Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, FL 32080.; Department of Biology, University of Florida, Gainesville, FL 32611., Martindale MQ; Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, FL 32080.; Department of Biology, University of Florida, Gainesville, FL 32611. |
| Abstrakt: |
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 C2H2-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). |
