Maternal vgll4a regulates zebrafish epiboly through Yap1 activity

Area of Science:

• Developmental Biology
• Cell Biology
• Genetics

Background:

• Zebrafish gastrulation involves epiboly, a cell spreading process relying on maternal transcripts.
• The regulation of yap1, a key mechano-transducer in epiboly, remains unclear.
• The maternal or zygotic origin of epiboly regulators is not fully understood.

Purpose of the Study:

• To investigate the role of maternal vgll4a in zebrafish epiboly.
• To determine how vgll4a affects yap1 activity and downstream targets.
• To elucidate the mechanism by which vgll4a influences cell adhesion and tissue mechanics during gastrulation.

Main Methods:

• Analysis of maternal/zygotic vgll4a (MZvgll4a) deficient zebrafish embryos.
• Assessment of epiboly progression and blastopore closure.
• Evaluation of yap1-downstream target gene expression.
• Investigation of actomyosin ring dynamics and E-cadherin/β-catenin complex localization.

Main Results:

• MZvgll4a deficient embryos exhibit delayed epiboly and blastopore closure.
• These embryos show altered cell morphology, reduced yap1 target gene expression, and impaired actomyosin ring function.
• vgll4a modulates E-cadherin/β-catenin complex levels, impacting actin cortex distribution, rather than directly competing with yap1.

Conclusions:

• Maternal vgll4a is essential for initiating zebrafish epiboly.
• vgll4a acts upstream of yap1 and the E-cadherin/β-catenin complex.
• Maternal vgll4a ensures a balance between tissue tension and contractility for timely epiboly progression.