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Reference Report
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| Citation | Winans, K.A., Hashimoto, C. (1995). Ventralization of the Drosophila embryo by deletion of extracellular leucine-rich repeats in the Toll protein. Mol. Biol. Cell 6(5): 587--596. (Export to RIS) | ||
| FlyBase ID | FBrf0082785 | ||
| Publication Type | Research paper | ||
| PubMed ID | 7663024 | ||
| PubMed Abstract | Dorsoventral polarity of the Drosophila embryo is established by a signal transduction pathway in which the maternal transmembrane protein Toll appears to function as the receptor for a ventrally localized extracellular ligand. Certain dominant Toll alleles encode proteins that behave as partially ligand-independent receptors, causing embryos containing these proteins to become ventralized. In extracts of embryos derived from mothers carrying these dominant alleles, we detected a polypeptide of approximately 35 kDa in addition to full-length Toll polypeptides with antibodies to Toll. Our biochemical analyses suggest that the smaller polypeptide is a truncated form of Toll lacking extracellular domain sequences. To assay the biological activity of such a shortened form of Toll, we synthesized RNA encoding a mutant polypeptide lacking the leucine-rich repeats that comprise most of Toll's extracellular domain and injected this RNA into embryos. The truncated Toll protein elicited the most ventral cell fate independently of the wild-type Toll protein and its ligand. These results support the view that Toll is a receptor whose extracellular domain regulates the intrinsic signaling activity of its cytoplasmic domain. | ||
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| Language of Publication | English | ||
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| Publication Type | Journal | ||
| Abbreviation | Mol. Biol. Cell | ||
| Title | Molecular Biology of the Cell | ||
| Publication Year | 1992- | ||
| ISBN/ISSN | 1059-1524 | ||
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Data from Reference
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| Aberrations (4)
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| Alleles (11)
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| Genes (5)
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