Reference Report
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| Citation | Gonzalez-Reyes, A., Elliott, H., St. Johnston, D. (1997). Oocyte determination and the origin of polarity in Drosophila: the role of the spindle genes. Development 124(24): 4927--4937. (Export to RIS) | ||
| FlyBase ID | FBrf0100046 | ||
| Publication Type | Research paper | ||
| PubMed ID | 9362456 | ||
| PubMed Abstract | The two main body axes in Drosophila become polarised as a result of a series of symmetry-breaking steps during oogenesis. Two of the sixteen germline cells in each egg chamber develop as pro-oocytes, and the first asymmetry arises when one of these cells is selected to become the oocyte. Anterior-posterior polarity originates when the oocyte then comes to lie posterior to the nurse cells and signals through the Gurken/Egfr pathway to induce the adjacent follicle cells to adopt a posterior fate. This directs the movement of the germinal vesicle and associated gurken mRNA from the posterior to an anterior corner of the oocyte, where Gurken protein signals for a second time to induce the dorsal follicle cells, thereby polarising the dorsal-ventral axis. Here we describe a group of five genes, the spindle loci, which are required for each of these polarising events. spindle mutants inhibit the induction of both the posterior and dorsal follicle cells by disrupting the localisation and translation of gurken mRNA. Moreover, the oocyte often fails to reach the posterior of mutant egg chambers and differentiates abnormally. Finally, double mutants cause both pro-oocytes to develop as oocytes, by delaying the choice between these two cells. Thus, these mutants reveal a novel link between oocyte selection, oocyte positioning and axis formation in Drosophila, leading us to propose that the spindle genes act in a process that is common to several of these events. | ||
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| Language of Publication | English | ||
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| Publication Type | Journal | ||
| Abbreviation | Development | ||
| Title | Development | ||
| Publication Year | 1987- | ||
| ISBN/ISSN | 0950-1991 | ||
Data from Reference
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Aberrations (4)
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Alleles (18)
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Genes (12)
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Insertions (1)
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