<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Maier D</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><funding>National Science Foundation</funding><pagination>205</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9858708</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Cellular differentiation relies on the highly conserved Notch signaling pathway. Notch activity induces gene expression changes that are highly sensitive to chromatin landscape. We address Notch gene regulation using &lt;i>Drosophila&lt;/i> as a model, focusing on the genetic and molecular interactions between the Notch antagonist Hairless and the histone chaperone Asf1. Earlier work implied that Asf1 promotes the silencing of Notch target genes via Hairless (H). Here, we generate a novel &lt;i>H&lt;/i>&lt;sup>Δ&lt;i>CT&lt;/i>&lt;/sup> allele by genome engineering. Phenotypically, &lt;i>H&lt;/i>&lt;sup>Δ&lt;i>CT&lt;/i>&lt;/sup> behaves as a Hairless gain of function allele in several developmental contexts, indicating that the conserved CT domain of H has an attenuator role under native biological contexts. Using several independe</pubmed_abstract><journal>Genes</journal><pubmed_title>Genetic and Molecular Interactions between &lt;i>H&lt;/i>&lt;sup>Δ&lt;i>CT&lt;/i>&lt;/sup>, a Novel Allele of the Notch Antagonist Hairless, and the Histone Chaperone Asf1 in &lt;i>Drosophila melanogaster&lt;/i>.</pubmed_title><pmcid>PMC9858708</pmcid><funding_grant_id>NA 427/5-1 and NA 427/6-1 to ACN</funding_grant_id><funding_grant_id>CA 178974 to RAK</funding_grant_id><funding_grant_id>MA 1328/11-1 to DM</funding_grant_id><funding_grant_id>R01 CA178974</funding_grant_id><funding_grant_id>MCBBSF grant #2114950 to RAK</funding_grant_id><pubmed_authors>Bauer M</pubmed_authors><pubmed_authors>Boger M</pubmed_authors><pubmed_authors>Scharpf J</pubmed_authors><pubmed_authors>Sanchez Jimenez A</pubmed_authors><pubmed_authors>Kovall RA</pubmed_authors><pubmed_authors>Fechner J</pubmed_authors><pubmed_authors>Maier D</pubmed_authors><pubmed_authors>Nagel AC</pubmed_authors><pubmed_authors>Preiss A</pubmed_authors><pubmed_authors>Yuan Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic and Molecular Interactions between &lt;i>H&lt;/i>&lt;sup>Δ&lt;i>CT&lt;/i>&lt;/sup>, a Novel Allele of the Notch Antagonist Hairless, and the Histone Chaperone Asf1 in &lt;i>Drosophila melanogaster&lt;/i>.</name><description>Cellular differentiation relies on the highly conserved Notch signaling pathway. Notch activity induces gene expression changes that are highly sensitive to chromatin landscape. We address Notch gene regulation using &lt;i>Drosophila&lt;/i> as a model, focusing on the genetic and molecular interactions between the Notch antagonist Hairless and the histone chaperone Asf1. Earlier work implied that Asf1 promotes the silencing of Notch target genes via Hairless (H). Here, we generate a novel &lt;i>H&lt;/i>&lt;sup>Δ&lt;i>CT&lt;/i>&lt;/sup> allele by genome engineering. Phenotypically, &lt;i>H&lt;/i>&lt;sup>Δ&lt;i>CT&lt;/i>&lt;/sup> behaves as a Hairless gain of function allele in several developmental contexts, indicating that the conserved CT domain of H has an attenuator role under native biological contexts. Using several independe</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-22T09:05:03.99Z</modification><creation>2025-04-05T22:49:29.086Z</creation></dates><accession>S-EPMC9858708</accession><cross_references><pubmed>36672946</pubmed><doi>10.3390/genes14010205</doi></cross_references></HashMap>