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Differential role of 14‐3‐3 family members in Xenopus development
Author(s) -
Lau Jeffrey M.C.,
Wu Chunlai,
Muslin Anthony J.
Publication year - 2006
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20816
Subject(s) - xenopus , biology , morpholino , microbiology and biotechnology , gastrulation , embryo , signal transduction , embryogenesis , genetics , gene , zebrafish
The 14‐3‐3 proteins are intracellular dimeric phosphoserine/threonine binding molecules that participate in signal transduction, checkpoint control, nutrient sensing, and cell survival pathways. Previous work established that 14‐3‐3 proteins are required in early Xenopus laevis development by modulating fibroblast growth factor signaling. Although this general requirement for 14‐3‐3 proteins in Xenopus early embryogenesis is established, there is no information about the specific role of individual 14‐3‐3 genes. Botanical studies previously demonstrated functional specificity among 14‐3‐3 genes during plant development. In this study, an antisense morpholino oligo microinjection approach was used to characterize the requirement for six specific 14‐3‐3 family members in Xenopus embryogenesis. Microinjection experiments followed by Western blot analysis showed that morpholinos reduced specific 14‐3‐3 protein levels. Embryos lacking specific 14‐3‐3 isoforms displayed unique phenotypic defects. In particular, reduction of 14‐3‐3 tau (τ) protein, and to a lesser extent, 14‐3‐3 epsilon (ϵ), resulted in embryos with prominent gastrulation and axial patterning defects and reduced mesodermal marker gene expression. In contrast, reduction of 14‐3‐3 zeta (ζ) protein caused no obvious phenotypic abnormalities. Reduction of 14‐3‐3 gamma (γ) protein resulted in eye defects without gastrulation abnormalities. Therefore, individual 14‐3‐3 genes have separable functions in vertebrate embryonic development. Developmental Dynamics 235:1761–1776, 2006. © 2006 Wiley‐Liss, Inc.