ck16, NR2F3, l(3)ck16, don, SVP1
transcription factor - orphan nuclear receptor - zinc finger - required for development of four of the eight photoreceptors that develop in each ommatidium of the eye, the R3/R4 pair and the R1/R6 pair - Stem cell-intrinsic, triggers temporal factor gradients that diversify intermediate neural progenitors in the larval brain
None of the polypeptides share 100% sequence identity.
746, 543 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\svp using the Feature Mapper tool.
Expression of svp is observed in the two anterior-most pairs of cardioblasts in abdominal hemisegments.
svp transcript is detected in the Pp3 neuroblast group (also known as Ppd15, Ppd16, Ppd18 and Ppd20).
svp expression is similar to that seen in the AE127 svp-lacZ line. Expression is observed from embryonic stage 11 in some of the heart progenitor cells. svp is later expressed in cardioblasts in a pattern complementary to the tin pattern in that the two pairs of svp-expressing cardioblasts do not express tin. Expression is also observed in the corpus allatum. Expression is also observed in dorsal somatic muscle and CNS.
Both svp transcripts are expressed in the same pattern during Malphighian tubule development. Expression is detected starting at embryonic stage 10 on one side of the outgrowing tubules, and during eversion, in a group of 6 to 8 cells in the tip region.
svp is expressed in two waves in the neuroblast NB5-6 of thorax during ventral nerve cord development.
svp is expressed in a subtype-specific fashion in the larval eye. In embryos, it is expressed in 8-10 immature photoreceptor cells. In the larva, it is expressed in the R6-specific photoreceptors of the Bolwig organ and is excluded from the R5 photoreceptors.
GBrowse - Visual display of RNA-Seq signalsView Dmel\svp in GBrowse 2
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.
Annotations CG11502 and CG18158 merged as CG11502 in release 3 of the genome annotation.
Source for merge of svp BcDNA:GH08189 was a shared cDNA ( date:030728 ).
Of eight EMS-induced alleles listed by Gausz, Gyurkovics, Bencze, Awad, Holden and Ish-Horowicz, 1981 only two are now existent (svp1 and svp2).
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
The expression pattern of proneural genes of the AS-C and neurogenic genes of the E(spl)-C are examined in the procephlon and a map of the cells is constructed.
svp embryos show no defects in the neuroblast pattern, developmental errors start when svp expression is extinguished from the neuroblasts. Fewer than normal eve positive cells join the growing EL neuronal cluster, late embryonic CNS shows widespread anatomical disorganisation of neuronal cell bodies, axon tracts and glia.
Four neuroblast molecular markers (svp, pros, en and ftz) have been used to demonstrate that some neuroblasts are homologous between insects (Drosophila and Schistocerca). They have similar position, time of formation and time of gene expression. Results suggest that evolution of the insect CNS has occurred in part through altering the neuroblast pattern and fate.
Different cell types within an ommatidium respond differently to misexpression of svp and the effect of misexpression can be modified by decreasing the ras signalling activity. This suggests an interaction between ras and svp in mediating cell fate decisions in the compound eye.
The svp product can bind to a variety of hormone response elements containing the repeat AGGTCA and modulates usp product-based signalling both in vitro and in vivo. Ectopic expression of svp in vivo leads to lethality at times corresponding to peaks of ecdysone expression. Concomitant overexpression of usp rescues the larva from the lethal effects of svp.
svp-mediated repression of ecdysone signalling can occur by both DNA binding competition and protein-protein interactions.
Ectopic expression of svp causes cell fate changes during ommatidial assembly, with R7 being transformed to R1-R6.
Expression analysed in CNS study of neuroblasts and ganglion mother cells, using an enhancer trap to reveal the expression pattern.
Evolutionary history for nuclear receptor genes, in which gene duplication events and swapping between domains of different origins took place, is studied.
Mutant clonal analysis reveals that svp is required for normal receptor cell development in photoreceptors 1, 3, 4 and 6.
Originally identified as recessive lethal mutations; independently identified by an enhancer-trap screen to be a gene expressed in a subset of neuroblasts in the embryonic CNS and also in a subset of photoreceptor-cell precursors in the developing compound eye. Mutant alleles die as embryos with normal cuticular morphology, but have alterations in numbers of eve-positive neurons in some neuroblast lineages. svp- clones in the eye produce abnormal ommatidia where photoreceptors R1, R3, R4 and R6 are transformed toward another photoreceptor R7. In addition, svp- ommatidia usually contain one to two extra photoreceptor cells. Mosaic studies show that transformation towards R7 is due to cell autonomous requirement in R1, R3, R4 and R6, whereas production of extra cell(s) is a secondary phenotype caused by lack of svp+ function in other cells, most likely in R3 and R4. Formation of some, but not all, R7-like cells in svp- ommatidia is dependent on sev+ function.