A novel gene, BENI is required for the convergent extension during Xenopus laevis gastrulation
| Autor: | Tatsuo Michiue, Masafumi Inui, Makoto Asashima, Akimasa Fukui, Koji Okabayashi, Motohiro Homma |
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| Rok vydání: | 2007 |
| Předmět: |
Brachyury
Indoles animal structures Morpholino Genetic Vectors Molecular Sequence Data Oligonucleotides Xenopus Ectoderm Xenopus Proteins Xbra Xenopus laevis medicine Animals Amino Acid Sequence Molecular Biology In Situ Hybridization Body Patterning DNA Primers Cell Nucleus Activin-like signaling Gene knockdown Nuclear localization signal (NLS) Base Sequence biology Reverse Transcriptase Polymerase Chain Reaction Convergent extension Gene Expression Profiling Gene Expression Regulation Developmental Galactosides Gastrula Sequence Analysis DNA Cell Biology biology.organism_classification Molecular biology Activins Gastrulation medicine.anatomical_structure BENI embryonic structures T-Box Domain Proteins Signal Transduction Developmental Biology |
| Zdroj: | Developmental Biology. 303:270-280 |
| ISSN: | 0012-1606 |
| DOI: | 10.1016/j.ydbio.2006.11.014 |
| Popis: | Activin-like signaling plays an important role in early embryogenesis. Activin A, a TGF-β family protein, induces mesodermal/endodermal tissues in animal cap assays. In a screen for genes expressed early after treatment with activin A, we isolated a novel gene, denoted as BENI (Brachyury Expression Nuclear Inhibitor). The BENI protein has a conserved domain at the N-terminus that contains a nuclear localization signal (NLS), and two other NLSs in the C-terminal domain. BENI mRNA was localized to the animal hemisphere at the gastrula stages and to ectoderm except for neural regions at stage 17; expression persisted until the tadpole stage. The overexpression of BENI caused gastrulation defects and inhibition of elongation of activin-treated animal caps with reduction of Xbra expression. Moreover, whole-mount in situ hybridization revealed reduced expression of Xbra in BENI mRNA-injected regions of gastrula embryos. Functional knockdown of BENI using an antisense morpholino oligonucleotide also resulted in an abnormal phenotype of embryos curling to the dorsal side, and excessive elongation of activin-treated animal caps without altered expression of mesodermal markers. These results suggested that BENI expression is regulated by activin-like signaling, and that this regulation is crucial for Xbra expression. |
| Databáze: | OpenAIRE |
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