S6, air8, hen, l(1)air8, M(1)7BC
Gene model reviewed during 5.52
None of the polypeptides share 100% sequence identity.
Ribosomal protein S6 is the major substrate of protein kinases in eukaryote ribosomes. The phosphorylation is stimulated by growth factors, tumor promoting agents, and mitogens. It is dephosphorylated at growth arrest.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\RpS6 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\RpS6 in GBrowse 2
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: RpS6 CG10944
Source for merge of RpS6 anon-WO02059370.61 was sequence comparison ( date:051113 ).
RNAi screen using dsRNA made from templates generated with primers directed against this gene results in aberrantly short, monopolar spindles when assayed in S2 cells. This phenotype can be observed when the screen is performed with or without Cdc27 dsRNA.
Deletions removing RpS6 but no other cytoplasmic ribosomal protein-encoding genes show Minute phenotypes.
Expression of transcript changes with adult age.
Mutants display a blood cell neoplastic phenotype.
Isolated from a Drosophila embryonic cDNA library using a human S6 cDNA as a probe, under intermediate stringency conditions.
Comparison of cDNA with genomic DNA identifies a transcription unit including three exons. Two tandem repeats downstream of this transcription unit reiterate divergent copies of the third exon and flanking regions. Comparison of these three repeats with respect to nucleotide sequence shows they clearly arose via a duplication and subsequent crossing over between misaligned copies. Although no direct evidence exists that the downstream exons are transcribed the maintenance of open reading frames in spite of extensive genetic changes is consistent with a protein-coding function.
Genetic and molecular analysis of RpS6 and phenotypic characterisation of two lethal mutations which result in hypertrophy of the larval haematopoietic organs because of overproliferation and aberrant development of haemocytes.
When mutated RpS6 causes overproliferation of the larval haemopoietic cells, tumour formation and an increase in the nuclear DNA content of haemopoietic cells.
Mutations cause overgrowth of lymph glands, abnormal blood cell differentiation, melanotic tumour formation, delayed larval growth, larval organ development retardation and larval death. Clonal analysis reveals wild type RpS6 required for clone survival in germ line and imaginal discs. Regulatory role of RpS6 in the hematopoeitic system may be related to its developmentally regulated phosphorylation.
A deficiency chromosome that removes RpS14A and RpS14B does not display the Minute phenotype associated with the M(1)7C locus: RpS14A and RpS14B do not correspond to the M(1)7C locus.
Mutations that exhibit melanotic tumor phenotypes have been initially characterized.
Deficiency mapping suggests that M(1)7C, a novel minute locus, is in the same region as RpS14A and RpS14B.
Dysgenic revertants were generated using jumpstarter mutagenesis for P-element excision.
One of a class of genes (see MIN record) that when present in one, rather than two, copies, produce a characteristic phenotype consisting of short slender bristles and delayed development.