jun, Djun, D-Jun, AP-1, c-Jun
transcription factor - basic leucine zipper - cooperates with the ETS domain protein Pointed to induce R7 fate in the developing eye - normal dendrite growth in Drosophila motor neurons requires the AP-1 (a Fos, Jun heterodimer) transcription factor
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Jra using the Feature Mapper tool.
Jra expression is generally consistent over this time period, with a peak at 0h APF.
Jra transcript is expressed in salivary glands from 18 hours prior to puparium formation to 12 hours APF. Expression peaks from the middle of the late larval ecdysone pulse though 2 hours APF.
Jra transcripts are detected at a relatively constant level throughout development on northern blots. In situ hybridization shows that they are expressed uniformly at a low level in all cell types.
Jra protein expression is widespread during embryogenesis. One tissue showing elevated Jra expression is the amnioserosa. During and following germ band retraction, the cells of the dorsal epidermis show elevated levels of Jra protein. The highest levels are found in the cells at the leading dorsal edge of the epidermis which are involved in the process of dorsal closure. Expression remains high in these cells throughout the process of dorsal closure. Elevated expression is also observed along the cephalic furrow.
Jra protein is expressed posterior to the morphogenetic furrow in all cells entering the ommatidial cluster including photoreceptor cells, cone cells and the mystery cell. Its expression is transient. It is expressed in the cells as they are newly recruited to the ommatidial cluster and for 3-4 columns posteriorly.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Jra 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.
Source for merge of: Jra l(2)46Ef
DNA-protein interactions: genome-wide binding profile assayed for Jra 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).
S2 cells treated with dsRNA generated against this gene show reduced phagocytosis of Candida albicans compared to untreated cells.
dsRNA made from templates generated with primers directed against this gene results in dorsal-closure defects in 79.4% of injected embryos.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Clonal analysis reveals that loss of function mutants cause defects in R3 induction and planar polarity determination, whereas gain of function mutants induce the R3 fate and associated polarity phenotypes.
Jra in the embryo is a downstream target of the bsk signal transduction pathway during dorsal closure formation. The function of the bsk/Jra pathway is to control the localised expression of dpp. Both in the embryo and during photoreceptor cell determination Jra is not regulated by a pathway that involved rl. Jra is required for the initiation of dorsal closure (controls the organisation of the leading edge cells), but not for embryonic segmentation or photoreceptor cell differentiation in the eye.
Transcription factors Jra and aop are required for dorsal closure. Results suggest that the bsk pathway governs dorsal closure at least partially by regulating dpp expression via phosphorylation of Jra and aop. Jra function is not required for the specification of cell fate in the eye.
Jra is a substrate for rl, part of the receptor tyrosine kinase signal transduction pathway which triggers photoreceptor differentiation during eye development. Mutant analysis implicates Jra phosphorylation in the choice between neuronal and non-neuronal fate during eye development.
Promoter deletion analysis of Jra-Ecol\CAT fusion constructs indicates that multiple cis-acting elements in the promoter region and the 5' non-coding region of the transcription unit control Jra expression.
The AP-1 complex encodes two proteins that have functional and structural properties in common with mammalian Fos and Jun proto-oncogene products; kay and Jra, respectively. The biochemical properties of the Jra gene product have been examined in vitro and the expression pattern in developing embryos studied.
Isolated from a genomic library using a human jun cDNA as a probe.