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

• Published in: Nature communications Vol. 9; no. 1; pp. 1319 - 16
• Main Authors: Williams, Margot L K, Sawada, Atsushi, Budine, Terin, Yin, Chunyue, Gontarz, Paul, Solnica-Krezel, Lilianna
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 03.04.2018; Nature Publishing Group UK; Nature Portfolio
• Subjects: Adhesion; Animals; Body Patterning; Cell Adhesion; Cell adhesion & migration; Cell adhesion molecules; Cell Communication; Chromatin; Chromatin - chemistry; Crosses, Genetic; Embryogenesis; Erythroid-Specific DNA-Binding Factors - genetics; Erythroid-Specific DNA-Binding Factors - physiology; Gastrulation; Gene expression; Gene Expression Regulation, Developmental; Membrane Glycoproteins - physiology; Morphogenesis; Mutants; Mutation; Notochord; Notochord - physiology; Pattern formation; Polarity; Sequence Analysis, RNA; Signal Transduction; Signaling; Xenopus; Zebrafish; Zebrafish Proteins - genetics; Zebrafish Proteins - physiology
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/s41467-018-03715-w

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.