Rpd3, dHDAC1, dRPD3, HDAC, l(3)04556
histone deacetylase. functioning in gene silencing - interacts with Groucho - required for starvation stress resistance - interacts with insulin signaling in Drosophila longevity extension
Please see the JBrowse view of Dmel\HDAC1 for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.46
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.56
2.2 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
521 (aa)
520 (aa)
Component of a form of the Esc/E(z) complex present specifically during early embryogenesis which is composed of Caf1-55, esc, E(z), Su(z)12, Pcl and HDAC1 (PubMed:12533794, PubMed:12408863, PubMed:12697833). The Esc/E(z) complex may also associate with Pcl and HDAC1 during early embryogenesis (PubMed:12697833). This complex is distinct from the PRC1 complex, which contains many other PcG proteins like Pc, Ph, Psc, Su(z)2 (PubMed:12533794). The 2 complexes however cooperate and interact together during the first 3 hours of development to establish PcG silencing (PubMed:12533794). Interacts with the histone methyltransferase Su(var)3-9 (PubMed:11571273). Component of a complex that contains at least HDAC1, CoRest and Su(var)3-3/Hdm (PubMed:15306652). Component of the DREAM complex at least composed of Myb, Caf1-55, mip40, mip120, mip130, E2f2, Dp, Rbf, Rbf2, lin-52, HDAC1 and l(3)mbt (PubMed:15545624). Interacts with the chromatin-remodeler Mi-2 (PubMed:18250149).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\HDAC1 using the Feature Mapper tool.
Comment: maternally deposited
GBrowse - Visual display of RNA-Seq signals
View Dmel\HDAC1 in GBrowse 2Maps near the tip of 3L.
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Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for identity of: HDAC1 Rpd3
Source for merge of: Rpd3 l(3)04556
Source for merge of: Rpd3 Su(var)328 Su(var)326
Source for merge of: Rpd3 l(3)64Cc
Renamed from 'Rpd3' to 'HDAC1' (a popular synonym) to be consistent with the naming convention of the other D. melanogaster HDAC genes (i.e. named after the mammalian orthologs).
DNA-protein interactions: genome-wide binding profile assayed for Rpd3 protein in Kc167 cells; see Chromatin_types_NKI collection report. Individual protein-binding experiments listed under "Samples" at GEO_GSE22069 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22069).
Gene expression is increased in response to the presence of two copies of Scer\GAL4hs.PB.
S2 cell populations treated with dsRNA made from templates generated with primers directed against Rpd3 show inhibition of cell growth due to a G2 arrest.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of Rpd3 results in increased arborization of ddaD and ddaE neurons, defects in muscle, defects in dendrite morphogenesis and reproducible defects in da dendrite development.
Rpd3 may be a component of the silencing complex for chromatin modification on specific regulatory regions of the homeotic genes.
Rpd3 is required for PRE-mediated silencing in vivo.
Specific missense mutations in Rpd3 suppress the silencing of genes subject to PEV, perhaps by acting as antimorphs that poisen the deacetylase complex.
Mutational analysis indicates that the Rpd3 histone deacetylase acts as a global transcriptional regulator.
The Rpd3 histone deacetylase is required for segmentation of the Drosophila embryo.
Loss of Rpd3 results in increased genomic silencing, which decreases the distance from heterochromatin.
Identified during a genetic analysis designed to identify mutations in the Dhc64C gene.
The autosomal "FLP-DFS" technique (using the P{ovoD1-18} P{FRT(whs)} P{hsFLP} chromosomes) has been used to identify the specific maternal effect phenotype for the zygotic lethal mutation.