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通过微阵列分析揭示U0126和成纤维细胞生长因子对玻璃海鞘胚胎基因表达谱的影响。

Effects of U0126 and fibroblast growth factor on gene expression profile in Ciona intestinalis embryos as revealed by microarray analysis.

作者信息

Sakabe Eriko, Tanaka Nobuhiko, Shimozono Naoki, Gojobori Takashi, Fujiwara Shigeki

机构信息

Department of Materials Science, Kochi University, Kochi-shi, Japan.

出版信息

Dev Growth Differ. 2006 Aug;48(6):391-400. doi: 10.1111/j.1440-169X.2006.00877.x.

Abstract

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.

摘要

成纤维细胞生长因子(FGF)通过属于丝裂原活化蛋白激酶(MAPK)家族的细胞外信号调节激酶(ERK),在海鞘胚胎中诱导脊索和间充质的形成。利用cDNA微阵列分析来鉴定被MAPK/ERK激酶(MEK)抑制剂U0126影响的海鞘Ciona intestinalis胚胎中的基因。从微阵列和原位杂交获得的数据表明,大多数基因在U0126处理后表达下调。在经U0126处理的胚胎中表达下调的基因包括Ci-Bra和Ci-Twist-like1,它们分别是脊索和间充质分化的主要调控基因。在预定内胚层细胞中,纤溶酶原mRNA在U0126处理后表达下调。这表明MEK介导的细胞外信号对于那些其特化不依赖细胞间相互作用的组织中的基因表达是必需的。在85个不受U0126影响的cDNA簇中,有30个在赤道区域的神经索/肌肉谱系卵裂球中显示出线粒体样mRNA定位。这些mRNA的表达水平和不对称分布与MEK信号传导无关。

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