<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fenelon KD</submitter><funding>UTA STARS</funding><pagination>1759</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11545809</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(21)</volume><pubmed_abstract>Transcriptional regulation, orchestrated by the interplay between transcription factors (TFs) and enhancers, governs gene expression dynamics crucial for cellular processes. While gross qualitative fluctuations in transcription factor-dependent gene expression patterning have a long history of characterization, the roles of these factors in the nuclei retaining expression in the presence or absence of these factors are now observable using modern techniques. Our study investigates the impact of Suppressor of Hairless (Su(H)), a broadly expressed transcription factor, on enhancer-driven transcriptional modulation using &lt;i>Drosophila&lt;/i> early embryos as a model system. Building upon previous findings, we employ super-resolution microscopy to dissect Su(H)'s influence on &lt;i>sog-Distal&lt;/i> (&lt;i>sogD&lt;/i>) enhancer activity specifically in nuclei with preserved &lt;i>sogD&lt;/i>-driven expression in the absence of Su(H) binding. We demonstrate that Su(H) occupancy perturbations alter expression levels and bursting dynamics. Notably, Su(H) absence during embryonic development exhibits region-specific effects, inhibiting expression dorsally and stabilizing expression ventrally, implying a nuanced role in enhancer regulation. Our findings shed light on the intricate mechanisms that govern transcriptional dynamics and suggest a critical patterning role for Notch/Hairless signaling in &lt;i>sog&lt;/i> expression as embryos transition to gastrulation.</pubmed_abstract><journal>Cells</journal><pubmed_title>Su(H) Modulates Enhancer Transcriptional Bursting in Prelude to Gastrulation.</pubmed_title><pmcid>PMC11545809</pmcid><funding_grant_id>123456</funding_grant_id><pubmed_authors>Fenelon KD</pubmed_authors><pubmed_authors>Borad P</pubmed_authors><pubmed_authors>Nasr MS</pubmed_authors><pubmed_authors>Koromila T</pubmed_authors><pubmed_authors>Luber JM</pubmed_authors><pubmed_authors>Rout B</pubmed_authors><pubmed_authors>Malidarreh PB</pubmed_authors></additional><is_claimable>false</is_claimable><name>Su(H) Modulates Enhancer Transcriptional Bursting in Prelude to Gastrulation.</name><description>Transcriptional regulation, orchestrated by the interplay between transcription factors (TFs) and enhancers, governs gene expression dynamics crucial for cellular processes. While gross qualitative fluctuations in transcription factor-dependent gene expression patterning have a long history of characterization, the roles of these factors in the nuclei retaining expression in the presence or absence of these factors are now observable using modern techniques. Our study investigates the impact of Suppressor of Hairless (Su(H)), a broadly expressed transcription factor, on enhancer-driven transcriptional modulation using &lt;i>Drosophila&lt;/i> early embryos as a model system. Building upon previous findings, we employ super-resolution microscopy to dissect Su(H)'s influence on &lt;i>sog-Distal&lt;/i> (&lt;i>sogD&lt;/i>) enhancer activity specifically in nuclei with preserved &lt;i>sogD&lt;/i>-driven expression in the absence of Su(H) binding. We demonstrate that Su(H) occupancy perturbations alter expression levels and bursting dynamics. Notably, Su(H) absence during embryonic development exhibits region-specific effects, inhibiting expression dorsally and stabilizing expression ventrally, implying a nuanced role in enhancer regulation. Our findings shed light on the intricate mechanisms that govern transcriptional dynamics and suggest a critical patterning role for Notch/Hairless signaling in &lt;i>sog&lt;/i> expression as embryos transition to gastrulation.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2025-04-04T18:56:09.089Z</modification><creation>2025-04-04T18:56:09.089Z</creation></dates><accession>S-EPMC11545809</accession><cross_references><pubmed>39513866</pubmed><doi>10.3390/cells13211759</doi></cross_references></HashMap>