Capicua integrates input from two maternal systems in Drosophila terminal patterning
In Drosophila, the maternal terminal system specifies cell fates at the embryonic poles via the localised stimulation of the Torso receptor tyrosine kinase (RTK). Signalling by the Torso pathway relieves repression mediated by the Capicua and Groucho repressors, allowing the restricted expression of...
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Published in | The EMBO journal Vol. 23; no. 23; pp. 4571 - 4582 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Chichester, UK
John Wiley & Sons, Ltd
24.11.2004
Blackwell Publishing Ltd Nature Publishing Group |
Subjects | |
Online Access | Get full text |
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Summary: | In Drosophila, the maternal terminal system specifies cell fates at the embryonic poles via the localised stimulation of the Torso receptor tyrosine kinase (RTK). Signalling by the Torso pathway relieves repression mediated by the Capicua and Groucho repressors, allowing the restricted expression of the zygotic terminal gap genes tailless and huckebein. Here we report a novel positive input into tailless and huckebein transcription by maternal posterior group genes, previously implicated in abdomen and pole cell formation. We show that absence of a subset of posterior group genes, or their overactivation, leads to the spatial reduction or expansion of the tailless and huckebein posterior expression domains, respectively. We demonstrate that the terminal and posterior systems converge, and that exclusion of Capicua from the termini of posterior group mutants is ineffective, accounting for reduced terminal gap gene expression in these embryos. We propose that the terminal and posterior systems function coordinately to alleviate transcriptional silencing by Capicua, and that the posterior system fine‐tunes Torso RTK signalling output, ensuring precise spatial domains of tailless and huckebein expression. |
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Bibliography: | istex:8D8E2E9C4DCCDF9CAD315C25D72B6DC0911739A9 ArticleID:EMBJ7600457 ark:/67375/WNG-S6NSKH2C-W ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 These authors contributed equally to this work |
ISSN: | 0261-4189 1460-2075 |
DOI: | 10.1038/sj.emboj.7600457 |