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Functional roles of Notch signaling in the cnidarian Nematostella vectensis

Authors :
Michiel Boekhout
Heather Marlow
Mark Q. Martindale
Eric Roettinger
Source :
Developmental Biology. (2):295-308
Publisher :
Elsevier Inc.

Abstract

Notch signaling is among the oldest of known Metazoan signaling pathways and is used in a multitude of developmental contexts to effect cellular differentiation, specification and the maintenance of stem cell state. Here we report the isolation and expression of the canonical Notch signaling pathway in the early branching metazoan Nematostella vectensis (Anthozoa, Cnidaria) during embryonic and larval development. We have used pharmacological treatment, morpholino knockdown, and dominant negative misexpression experiments to demonstrate that Notch signaling acts to mediate cnidogenesis, the development of cnidarian-specific neural effecter cells. Notch signaling often results in the transcriptional activation of NvHes genes, a conserved family of bHLH transcription factors. A loss of Notch signaling through use of pharmacological inhibition or knock-down of the Notch effecter gene Suppressor of Hairless Su(H) similarly results in a loss of cnidocyte cell fate. We also provide evidence that Notch signaling is responsible for certain aspects of neurogenesis in developing N. vectensis planula in which disruption of Notch cleavage via the pharmacological agent DAPT results in increased expression of neural marker genes in vivo. This data suggests that Notch signaling acting on components of the developing nervous system is an ancient role of this pathway. The shared requirement of Notch signaling for the development of both cnidocytes and neurons further supports the hypothesis that cnidocytes and neurons share common origins as multifunctional sensory-effecter cells.

Details

Language :
English
ISSN :
00121606
Issue :
2
Database :
OpenAIRE
Journal :
Developmental Biology
Accession number :
edsair.doi.dedup.....958a94b93809bf88a6933c7f4bcca2ea
Full Text :
https://doi.org/10.1016/j.ydbio.2011.11.012