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Gon4l regulates notochord boundary formation and cell polarity underlying axis extension by repressing adhesion genes

Margot L. K. Williams,A. Sawada,Terin Budine,Chunyue Yin,P. Gontarz,L. Solnica-Krezel

Published 2018 in Nature Communications

ABSTRACT

Anteroposterior (AP) axis extension during gastrulation requires embryonic patterning and morphogenesis to be spatiotemporally coordinated, but the underlying genetic mechanisms remain poorly understood. Here we define a role for the conserved chromatin factor Gon4l, encoded by ugly duckling (udu), in coordinating tissue patterning and axis extension during zebrafish gastrulation through direct positive and negative regulation of gene expression. Although identified as a recessive enhancer of impaired axis extension in planar cell polarity (PCP) mutants, udu functions in a genetically independent, partially overlapping fashion with PCP signaling to regulate mediolateral cell polarity underlying axis extension in part by promoting notochord boundary formation. Gon4l limits expression of the cell–cell and cell–matrix adhesion molecules EpCAM and Integrinα3b, excesses of which perturb the notochord boundary via tension-dependent and -independent mechanisms, respectively. By promoting formation of this AP-aligned boundary and associated cell polarity, Gon4l cooperates with PCP signaling to coordinate morphogenesis along the AP embryonic axis.Anteroposterior axis extension during gastrulation is dynamically coordinated, but how this is regulated at a molecular level is unclear. Here, the authors show in zebrafish that the chromatin factor Gon4l, encoded by ugly duckling, coordinates axis extension by modulating EpCAM and Integrinα3b expression.

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