z-logo
Premium
Effects of U0126 and fibroblast growth factor on gene expression profile in Ciona intestinalis embryos as revealed by microarray analysis
Author(s) -
Sakabe Eriko,
Tanaka Nobuhiko,
Shimozono Naoki,
Gojobori Takashi,
Fujiwara Shigeki
Publication year - 2006
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/j.1440-169x.2006.00877.x
Subject(s) - notochord , biology , ciona intestinalis , mapk/erk pathway , microbiology and biotechnology , ciona , microarray analysis techniques , endoderm , fibroblast growth factor , gene expression , kinase , gene , embryo , cellular differentiation , genetics , embryogenesis , receptor
Fibroblast growth factor (FGF) induces the notochord and mesenchyme in ascidian embryos, via extracellular signal‐regulated kinase (ERK) that belongs to the mitogen‐activated protein kinase (MAPK) family. A cDNA microarray analysis was carried out to identify genes affected by an inhibitor of MAPK/ERK kinase (MEK), U0126, in embryos of the ascidian Ciona intestinalis . Data obtained from the microarray and in situ hybridization suggest that the majority of genes are downregulated by U0126 treatment. Genes that were downregulated in U0126‐treated embryos included Ci‐Bra and Ci‐Twist‐like1 that are master regulatory genes of notochord and mesenchyme differentiation, respectively. The plasminogen mRNA was downregulated by U0126 in presumptive endoderm cells. This suggests that a MEK‐mediated extracellular signal is necessary for gene expression in tissues whose specification does not depend on cell‐to‐cell interaction. Among 85 cDNA clusters that were not affected by U0126, 30 showed mitochondria‐like mRNA localization in the nerve cord/muscle lineage blastomeres in the equatorial region. The expression level and asymmetric distribution of these mRNA were independent of MEK signaling.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here