ArticleDevelopment (Cambridge, England)2022
Shadow enhancers modulate distinct transcriptional parameters that differentially effect downstream patterning events.
Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mitotic reactivation and transcriptional bursting govern transcriptional noise in the early Drosophila embryo.Development (Cambridge, England) · 2026Article
- Coordinated active repression operates via transcription factor cooperativity and multiple inactive promoter states in a developing organism.Nature communications · 2025Article
- Multiple cis-regulatory modules ensure robust tup/islet1 function in dorsal muscle identity specification.Skeletal muscle · 2025Article
- Biological roles of enhancer RNA m6A modification and its implications in cancer.Cell communication and signaling : CCS · 2025Review
- Optogenetic manipulation of nuclear Dorsal reveals temporal requirements and consequences for transcription.Development (Cambridge, England) · 2025Article
- A simple MiMIC-based approach for tagging endogenous genes to visualise live transcription in Drosophila.Development (Cambridge, England) · 2024Article
- Optogenetic manipulation of nuclear Dorsal reveals temporal requirements and consequences for transcription.bioRxiv : the preprint server for biology · 2024Article
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5 authors.
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Abstract
Transcription in the early Drosophila blastoderm is coordinated by the collective action of hundreds of enhancers. Many genes are controlled by so-called 'shadow enhancers', which provide resilience to environment or genetic insult, allowing the embryo to robustly generate a precise transcriptional pattern. Emerging evidence suggests that many shadow enhancer pairs do not drive identical expression patterns, but the biological significance of this remains unclear. In this study, we characterize the shadow enhancer pair controlling the gene short gastrulation (sog). We removed either the intronic proximal enhancer or the upstream distal enhancer and monitored sog transcriptional kinetics. Notably, each enhancer differs in sog spatial expression, timing of activation and RNA Polymerase II loading rates. In addition, modeling of individual enhancer activities demonstrates that these enhancers integrate activation and repression signals differently. Whereas activation is due to the sum of the two enhancer activities, repression appears to depend on synergistic effects between enhancers. Finally, we examined the downstream signaling consequences resulting from the loss of either enhancer, and found changes in tissue patterning that can be explained by the differences in transcriptional kinetics measured.
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