JIL1, Su(var)3-1, Suppressor of variegation 3-1, Su-var(3)1, MSK
protein serine/threonine kinase involved in dosage compensation - phosphorylates the His3 Serine 10 residue - antagonizes heterochromatization - regulates levels of gene expression by controlling the distribution of the epigenetic histone His3 Lysine 9 dimethylation
Please see the JBrowse view of Dmel\JIL-1 for information on other features
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Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.45
Tissue-specific extension of 3' UTRs observed during later stages (FBrf0218523, FBrf0219848); all variants may not be annotated
Interacts with lola. Interacts with proteins of the male specific lethal (MSL) dosage compensation complex; this interaction is mediated by the kinase domains.
Autophosphorylated in vitro.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\JIL-1 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signals
View Dmel\JIL-1 in GBrowse 23-34
3-34
3-28.4
3-
3-31.4 +/- 0.8
3-31.4
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
monoclonal
Source for identity of: JIL-1 CG6297
Source for merge of: JIL-1 Su(var)3-1
Source for merge of: JIL-1 anon-WO0118547.379
Source for merge of JIL-1 anon-WO0118547.379 was sequence comparison ( date:051113 ).
Loss of function mutations in JIL-1 are strong suppressors of position effect variegation.
The COOH-terminal domain of the JIL-1 product is required for correct chromosome localization.
When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, an increase in the proportion of G1 phase cells is seen.
JIL-1 has a role in controlling heterochromatin compaction and expansion.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Area matching Drosophila EST AA246367. This EST has sequence similarity to human ribosome S6 PK gene.
JIL-1 may play a role in transcriptional control, potentially by regulating chromatin structure.
Isolated in an expression library screen using monoclonal antibody 2A (mAb2A).
Mutations exhibit a small discs phenotype.