Ubiquitous overexpression of a transgene encoding the extracellular portion of the Drosophila Roughest-Irregular Chiasm C protein induces early embryonic lethality
| Autor: | Ricardo Guelerman Pinheiro Ramos, Ricardo C. Machado, Lívia Maria Rosatto Moda |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2000 |
| Předmět: |
Male
Embryo Nonmammalian Hot Temperature Cell Adhesion Molecules Neuronal Transgene Genes Insect transgenic organisms Biology immunoglobulin superfamily Pigment cell differentiation Extracellular Animals Drosophila Proteins Transgenes Eye Proteins Cell adhesion lcsh:Science Multidisciplinary Cell adhesion molecule Wild type Gene Expression Regulation Developmental Shock cell adhesion Molecular biology Embryonic stem cell Drosophila melanogaster Phenotype Insect Proteins Immunoglobulin superfamily Female Genes Lethal lcsh:Q Drosophila |
| Zdroj: | Anais da Academia Brasileira de Ciências, Volume: 72, Issue: 3, Pages: 381-388, Published: SEP 2000 Anais da Academia Brasileira de Ciências v.72 n.3 2000 Anais da Academia Brasileira de Ciências Academia Brasileira de Ciências (ABC) instacron:ABC Anais da Academia Brasileira de Ciências, Vol 72, Iss 3, Pp 381-388 (2000) |
| Popis: | The cell adhesion molecule Rst-irreC is a transmembrane glycoprotein of the immunoglobulin superfamily involved in several important developmental processes in Drosophila, including axonal pathfinding in the optic lobe and programmed cell death and pigment cell differentiation in the pupal retina. As an initial step towards the "in vivo'' functional analysis of this protein we have generated transgenic fly stocks carrying a truncated cDNA construct encoding only the extracellular domain of Rst-IrreC under the transcriptional control of the heat shock inducible promoter hsp70. We show that heat-shocking embryos bearing the transgene during the first 8hs of development lead to a 3-4 fold reduction in their viability compared to wild type controls. The embryonic lethality can already be produced by applying the heat pulse in the first 3hs of embryonic development, does not seem to be suppressed in the absence of wildtype product and is progressively reduced as the heat treatment is applied later in embryogenesis. These results are compatible with the hypothesis of the lethal phenotype being primarily due to heterophilic interactions between Rst-IrreC extracellular domain and an yet unknown ligand. |
| Databáze: | OpenAIRE |
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