Notch-mediated lateral inhibition is an evolutionarily conserved mechanism patterning the ectoderm in echinoids
- Creators
- Erkenbrack, Eric M.
Abstract
Notch signaling is a crucial cog in early development of euechinoid sea urchins, specifying both non-skeletogenic mesodermal lineages and serotonergic neurons in the apical neuroectoderm. Here, the spatial distributions and function of delta, gcm, and hesc, three genes critical to these processes in euechinoids, are examined in the distantly related cidaroid sea urchin Eucidaris tribuloides. Spatial distribution and experimental perturbation of delta and hesc suggest that the function of Notch signaling in ectodermal patterning in early development of E. tr ibuloides is consistent with canonical lateral inhibition. Delta transcripts were observed in t he archenteron, apical ectoderm, and lateral ectoderm in gastrulating e mbryos of E. tribuloides. Perturbation of Notch signaling by either delta morpholino or treatment of DAPT downregulated hesc and upregulated delta and gcm, resulting in ectopic expression of delta and gcm. Similarly, hesc perturbation mirrored the effects of delta perturbation. Interestingly, perturbation of delta or hesc resulted in more cells expressing gcm and supernumerary pigment cells, suggesting that pigment cell proliferation is regulated by Notch in E. tribuloides. These results are consistent with an evolutionary scenario whereby, in the echinoid ancestor, Notch signaling was deployed in the ectoderm to specify neurogenic progenitors and controlled pigment cell proliferation in the dorsal ectoderm.
Additional Information
© 2017 Springer-Verlag GmbH Germany, part of Springer Nature. Received: 12 June 2017; Accepted: 8 December 2017; First Online: 16 December 2017. Experimental data presented here were collected in the dungeon of the late Eric H. Davidson, who, along with Dave Bottjer, enthusiastically supported me and my research efforts. The manuscript was written in the laboratory of Günter P. Wagner, whose support and patience I appreciatively acknowledge. Comments from two anonymous reviewers greatly improved this manuscript. This research was supported by NSF grant IOS1240626. Another one.Attached Files
Supplemental Material - 427_2017_599_MOESM1_ESM.docx
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Additional details
- Eprint ID
- 83957
- Resolver ID
- CaltechAUTHORS:20171219-092236326
- IOS-1240626
- NSF
- Created
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2017-12-19Created from EPrint's datestamp field
- Updated
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2021-11-15Created from EPrint's last_modified field