Eaf1 and Eaf2 mediate zebrafish dorsal-ventral axis patterning via suppressing Wnt/β-Catenin activity

Area of Science:

• Developmental Biology
• Molecular Genetics
• Cell Signaling

Background:

• Maternal Wnt/β-catenin signaling is crucial for initiating dorsal gene expression in early vertebrate embryogenesis.
• The precise molecular mechanisms controlling dorsal-ventral patterning remain incompletely understood.

Purpose of the Study:

• To investigate the roles of Eaf1 and Eaf2 in modulating Wnt signaling during vertebrate embryogenesis.
• To elucidate the involvement of Eaf1 and Eaf2 in the specification of dorsal and ventral cell fates.

Main Methods:

• Analysis of maternal and zygotic knockout/mutant zebrafish (Danio rerio) models for eaf1 and eaf2.
• Overexpression studies of eaf1 and eaf2 in zebrafish embryos.
• Assessment of gene expression for ventral markers (ved, vent, vox) and dorsal marker (axin2) using quantitative methods.
• Investigation of Wnt/β-catenin signaling pathways (β-catenin1 and β-catenin2) and Tcf transcription factors.

Main Results:

• Eaf1 and Eaf2 act as maternal and zygotic modulators of Wnt signaling, influencing the initiation and specification of ventral genes.
• Loss of Eaf1/Eaf2 function enhances ventral gene expression, while overexpression suppresses it.
• Eaf1/Eaf2 suppress ventral fates via Wnt/β-catenin1/Tcf signaling and dorsal fates via Wnt/β-catenin2 signaling.
• Eaf1/Eaf2 inhibit β-catenin2-induced axin2 expression, particularly on the dorsal side.

Conclusions:

• Eaf1 and Eaf2 establish a novel dorsal-ventral patterning pathway in vertebrate embryogenesis.
• These proteins inhibit ventral cell development by suppressing Wnt/β-catenin1/Tcf signaling.
• Eaf1 and Eaf2 indirectly induce dorsal cell development by suppressing β-catenin2-induced axin2 expression dorsally.