The glucose-sensing transcription factor MondoA regulates zebrafish epiboly via cholesterol biosynthesis genes including the human disease gene Nsdhl, revealing an unknown role for metabolic glucose signalling in vertebrate development.

Rab25a and Rab25b mutant embryos exhibit epithelial spreading delays during morphogenesis and are characterized by cytokinesis defects leading to cell fusions, heterogeneous epithelial cell sizes, and reduced cortical actomyosin contractility.

Developing oocytes lacking Sphk2 sense high sphingosine levels and transcriptionally activate expression of the gene encoding Cers2b, to mediate a salvage pathway to reduce potentially toxic sphingosine.

Zebrafish embryo screen utilizing conserved mechanisms between cancer metastasis and zebrafish gastrulation identifies the HTR2C inhibitor pizotifen as anti-metastasis drugs.

Sec14l3/SEC14L2 respond to upstream Wnt/Frizzled/Dvl stimulation to recruit and activate phospholipase Cδ4a (Plcδ4a) to further initiate calcium release.

Screening for drugs that disrupt embryonic development in zebrafish can help identify treatments that suppress metastasis.

Different combinations of the transcription factors Pou5f3, Nanog and Sox32 form complexes to drive dorsoventral mesendoderm patterning in zebrafish.

Global gene expression analysis defines the transcriptional events during the development of zebrafish from fertilised egg to fully formed organism.

Expression of Pitx2c at the onset of gastrulation drives convergence and extension movements in the zebrafish embryo by promoting downstream pathways affecting chemokine signaling, integrin-ECM interactions, and planar cell polarity components.

Incomplete delamination serves as a cellular platform for coordinated tissue movements during development, guiding newly formed progenitor cell groups to the differentiation site.