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Published June 2001 | Published
Journal Article Open

LvNotch signaling plays a dual role in regulating the position of the ectoderm-endoderm boundary in the sea urchin embryo

Abstract

The molecular mechanisms guiding the positioning of the ectoderm-endoderm boundary along the animal-vegetal axis of the sea urchin embryo remain largely unknown. We report here a role for the sea urchin homolog of the Notch receptor, LvNotch, in mediating the position of this boundary. Overexpression of an activated form of LvNotch throughout the embryo shifts the ectoderm-endoderm boundary more animally along the animal-vegetal axis, whereas expression of a dominant negative form shifts the border vegetally. Mosaic experiments that target activated and dominant negative forms of LvNotch into individual blastomeres of the early embryo, combined with lineage analyses, further reveal that LvNotch signaling mediates the position of this boundary by distinct mechanisms within the animal versus vegetal portions of the embryo. In the animal region of the embryo, LvNotch signaling acts cell autonomously to promote endoderm formation more animally, while in the vegetal portion, LvNotch signaling also promotes the ectoderm-endoderm boundary more animally, but through a cell non-autonomous mechanism. We further demonstrate that vegetal LvNotch signaling controls the localization of nuclear β-catenin at the ectoderm-endoderm boundary. Based on these results, we propose that LvNotch signaling promotes the position of the ectoderm-endoderm boundary more animally via two mechanisms: (1) a cell-autonomous function within the animal region of the embryo, and (2) a cell non-autonomous role in the vegetal region that regulates a signal(s) mediating ectoderm-endoderm position, possibly through the control of nuclear β-catenin at the boundary.

Additional Information

© 2001 The Company of Biologists Limited. Accepted 29 March 2001. We thank C. Logan, A. Ransick and A. Wikramanayake for their suggestions on lineage labeling and micromanipulation. We also thank E. Davidson, G. Hong and P. Sternberg for supporting the completion of this work. Furthermore, we are grateful to N. Sherwood, R. Fehon, J. Gross and members of the McClay laboratory for invaluable discussions and advice throughout this work. This research was supported by Sigma Xi Grants-in-Aid of Research awards to D. R. S., NIH grant HD14483 to D. R. M. and NSF equipment grant BIR-9318118.

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