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Phosphatidylinositol 3-kinase (PI3 kinase) mediates gastrulation cell migration in zebrafish via its regulation of PIP 2 /PIP 3  balance. Although PI3 kinase counter enzyme PTEN has also been reported to be essential for gastrulation, its role in zebrafish gastrulation has been controversial due to the lack of gastrulation defects in  pten -null mutants. To clarify this issue, we knocked down a  pten  isoform,  ptenb  by using anti-sense morpholino oligos (MOs) in zebrafish embryos and found that  ptenb  MOs inhibit convergent extension by affecting cell motility and protrusion during gastrulation. The  ptenb  MO-induced convergence defect could be rescued by a PI3-kinase inhibitor, LY294002 and by overexpressing dominant negative Cdc42. Overexpression of human constitutively active  akt1  showed similar convergent extension defects in zebrafish embryos. We also observed a clear enhancement of actin polymerization in  ptenb  morphants under cofocal microscopy and in actin polymerization assay. These results suggest that Ptenb by antagonizing PI3 kinase and its downstream Akt1 and Cdc42 to regulate actin polymerization that is critical for proper cell motility and migration control during gastrulation in zebrafish.

Ptenb Mediates Gastrulation Cell Movements via Cdc42/AKT1 in Zebrafish