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Published January 11, 2011 | Supplemental Material + Accepted Version
Journal Article Open

Zebrafish Neural Tube Morphogenesis Requires Scribble-Dependent Oriented Cell Divisions

Abstract

How control of subcellular events in single cells determines morphogenesis on the scale of the tissue is largely unresolved. The stereotyped cross-midline mitoses of progenitors in the zebrafish neural keel [1–4] provide a unique experimental paradigm for defining the role and control of single-cell orientation for tissue-level morphogenesis in vivo. We show here that the coordinated orientation of individual progenitor cell division in the neural keel is the cellular determinant required for morphogenesis into a neural tube epithelium with a single straight lumen. We find that Scribble is required for oriented cell division and that its function in this process is independent of canonical apicobasal and planar polarity pathways. We identify a role for Scribble in controlling clustering of α-catenin foci in dividing progenitors. Loss of either Scrib or N-cadherin results in abnormally oriented mitoses, reduced cross-midline cell divisions, and similar neural tube defects. We propose that Scribble-dependent nascent cell-cell adhesion clusters between neuroepithelial progenitors contribute to define orientation of their cell division. Finally, our data demonstrate that while oriented mitoses of individual cells determine neural tube architecture, the tissue can in turn feed back on its constituent cells to define their polarization and cell division orientation to ensure robust tissue morphogenesis.

Additional Information

© 2011 Elsevier Ltd. Received: July 9, 2010, Revised: October 18, 2010, Accepted: December 2, 2010, Published online: December 23, 2010. We thank L. Solnica-Krezel and H. Okamoto for zebrafish lines and B. Ciruna, H. Wada, M. Halloran, and S. Megason for plasmids. We are grateful for K. Guthrie for assistance with statistical analysis. A. Kohlmaier, C. Tsiairis, V. Vasioukhin, and members of the C.B.M. laboratory are acknowledged for their comments on the manuscript. Work in the S.E.F. laboratory was supported by National Human Genome Research Institute Center of Excellence in Genomic Science grant P50HG004071. This work was supported by National Institutes of Health grant HD37909 to C.B.M. C.B.M. is an investigator of the Howard Hughes Medical Institute.

Attached Files

Accepted Version - Zigman2011p12740Curr_Biol.pdf

Accepted Version - nihms262663.pdf

Supplemental Material - mmc1.pdf

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Created:
August 19, 2023
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October 23, 2023