ArticleNucleic acids research2009
The Torso signaling pathway modulates a dual transcriptional switch to regulate tailless expression.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- OVO positively regulates essential maternal pathways by binding near the transcriptional start sites in theeLife · 2024Article
- OVO Positively Regulates Essential Maternal Pathways by Binding Near the Transcriptional Start Sites in thebioRxiv : the preprint server for biology · 2024Article
- Global repression by tailless during segmentation.Developmental biology · 2024Article
- Histone deacetylase (Rpd3) regulatesOpen biology · 2020Article
- Pits, a protein interacting with Ttk69 and Sin3A, has links to histone deacetylation.Scientific reports · 2016Article
- Identification of an intronic cis-acting element in the human dopamine transporter gene.Molecular biology reports · 2012Article
- The gap gene network.Cellular and molecular life sciences : CMLS · 2011Review
- A tale of tailless.Developmental neuroscience · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Torso (Tor) signaling pathway activates tailless (tll) expression by relieving tll repression. None of the repressors identified so far, such as Capicuo, Groucho and Tramtrack69 (Ttk69), bind to the tor response element (tor-RE) or fully elucidate tll repression. In this study, an expanded tll expression pattern was shown in embryos with reduced heat shock factor (hsf) and Trithorax-like (Trl) activities. The GAGA factor, GAF encoded by Trl, bound weakly to the tor-RE, and this binding was enhanced by both Hsf and Ttk69. A similar extent of expansion of tll expression was observed in embryos with simultaneous knockdown of hsf, Trl and ttk69 activities, and in embryos with constitutively active Tor. Hsf is a substrate of mitogen-activated protein kinase and S378 is the major phosphorylation site. Phosphorylation converts Hsf from a repressor to an activator that works with GAF to activate tll expression. In conclusion, the GAF/Hsf/Ttk69 complex binding to the tor-RE remodels local chromatin structure to repress tll expression and the Tor signaling pathway activate tll expression by modulating a dual transcriptional switch.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.