ArticleDevelopmental cell2014
An enhancer composed of interlocking submodules controls transcriptional autoregulation of suppressor of hairless.
Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- The Drosophila histone variant H2Av facilitates Notch signaling activity in a two-tier regulatory fashion.Cell communication and signaling : CCS · 2025Article
- Article
- Positive autoregulation ofDevelopment (Cambridge, England) · 2020Article
- Shaping ofGenetics · 2019Article
- Mutational analysis of a Drosophila neuroblast enhancer governing nubbin expression during CNS development.Genesis (New York, N.Y. : 2000) · 2018Article
- A Drosophila Tumor Suppressor Gene Prevents Tonic TNF Signaling through Receptor N-Glycosylation.Developmental cell · 2018Article
- Short-Form Bomanins Mediate Humoral Immunity in Drosophila.Journal of innate immunity · 2018Article
- The Canonical Notch Signaling Pathway: Structural and Biochemical Insights into Shape, Sugar, and Force.Developmental cell · 2017Review
- Negative control of CSL gene transcription by stress/DNA damage response and p53.Cell cycle (Georgetown, Tex.) · 2016Article
- A composite enhancer regulates p63 gene expression in epidermal morphogenesis and in keratinocyte differentiation by multiple mechanisms.Nucleic acids research · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Positive autoregulation is an effective mechanism for the long-term maintenance of a transcription factor's expression. This strategy is widely deployed in cell lineages, where the autoregulatory factor controls the activity of a battery of genes that constitute the differentiation program of a postmitotic cell type. In Drosophila, the Notch pathway transcription factor Suppressor of Hairless activates its own expression, specifically in the socket cell of external sensory organs, via an autoregulatory enhancer called the ASE. Here, we show that the ASE is composed of several enhancer submodules, each of which can independently initiate weak Su(H) autoregulation. Cross-activation by these submodules is critical to ensure that Su(H) rises above a threshold level necessary to activate a maintenance submodule, which then sustains long-term Su(H) autoregulation. Our study reveals the use of interlinked positive-feedback loops to control autoregulation dynamically and provides mechanistic insight into initiation, establishment, and maintenance of the autoregulatory state.
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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.