MAPK, ERK, dpERK, MAP kinase, pERK
Component of Epidermal growth factor receptor signaling pathway - involved in establishment of the dorsoventral polarity of the egg shell and the embryo - acts in specification of terminal structures immediately after fertilization - Gain-of-function mutants produce extra R7 photoreceptors and extra wing veins
Gene model reviewed during 5.47
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.44
Gene model reviewed during 5.55
2.6 (longest cDNA)
376 (aa); 44 (kD observed)
Antibody made to phosphorylated Erk
rl protein was shown to phosphorylate Jra protein in Drosophila. The substrates for rl protein were identified as Jra residues Ser82, Thr92 and Thr107 in vitro. Ser82 and Thr92 were shown to be in vivo targets as well and Thr 107 was weakly labelled both in vitro and in vivo.
Dually phosphorylated on Thr-198 and Tyr-200, which activates the enzyme (By similarity). Phosphorylated on tyrosine residue(s) in response to insulin.
The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\rl using the Feature Mapper tool.
At embryonic stage 15, an antibody to the phosphorylated form of rl stains pericardial precursor cells, several muscle cells, and ectodermal muscle attachment cells.
Activated rl (MAPK) is first detected along the dorsal midline of the follicular epithelium at oogenesis stage S9/10. At stage 10A it is found in two dorsolateral patches of the follicular epithelium, excluding a triangular region near the oocyte nucleus. At stage 10B, it is found in two L-shaped domains at the dorsoanterior region of the follicular epithelium but not in posterior regions. The pattern of activated rl (MAPK) staining was compared across Drosophila subgenera.
Diphosphorylated rl is expressed in a male-specific manner in posterior somatic gonadal precursors in the embryo.
Expression of rl in the leg disc in a central distal domain after 72 hr AEL. At 96 hr AEL, a dorsal femoral cluster starts to form, plus a dynamic pattern of cells scattered over the disc (presumable sensory organs) is observed. By 120 hr AEL, the pattern resembles rho expression with rings in every segment, twin femoral clusters, and no clear pretarsal cluster. In contrast to rho, the domains do not extend across the segmental folds.
Expression of phosphorylated rl protein is observed in the dorsal pharyngeal head mesoderm, and later in the three invaginations of the developing stomatogastric nervous system.
rl protein was observed inboth the nucleus and the cytoplasm of S2 cells. In about 10% of thestained cells, rl protein was excluded from the nucleus. Inphotoreceptor cells, rl protein is observed in the cytoplasm.
rl protein is observed in the invaginated mesoderm in cells that contact the ectoderm and later in cells at the leading edge of the mesoderm as it spreads over the ectoderm. It is observed in tracheal cells as migration begins.
An antibody to the double phosphorylated form of rl was used in these experiments. Prominent staining at both poles is detected at cycle 13/14. At stage 8, expression is observed in the dorsal-most 3-4 rows of the mesoderm and is later restricted to the dorsal-most 1-2 rows. At stage 10, expression is observed in the tracheal placodes and then at stage 11 is seen broadly in the tracheal pits. As migration of the branch tips begins, expression is observed in the migrating tip cells. Prominent staining is observed in the visceral mesoderm at stage 11. It is first seen as segmental patches, before fusion of the visceral arches from each segment, and is subsequently observed as a continuous waved line. Finally, staining is observed at stage 15 in several muscle attachment cells on the ectoderm and in the ventral transverse muscles (VT1).
GBrowse - Visual display of RNA-Seq signalsView Dmel\rl 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 rl BcDNA:RE08694 was a shared cDNA ( date:030728 ).
dsRNA made from templates generated with primers directed against this gene.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
A gradient of rl activity controls differential gene expression and the establishment of various cell fates.
The rl gene product may regulate microtubule behavior during mitosis and mediate the checkpoint that assesses the integrity of the mitotic spindle.
The MAPK cascade is required for Ras85D mitogenic response, loss of function mutations in phl, Dsor1, rl and ksr dominantly suppress hyperplastic growth, as do mutations in the Ras85D effector loop that disrupt the Ras85D-phl interaction.
Phylogenetic and functional relationships of MAPKs is studied based on 93 non-redundant full length sequences, 2 atomic structures and known functions of MAPKs.
rl undergoes polytenization in salivary gland chromosomes to a degree comparable to that of euchromatic genes, despite its deep heterochromatic location. Bari1 sequences located to the left are severely underrepresented and thus appear to be α-heterochromatin. rl is transcribed in polytene tissues. Together these results indicate that functional sequences located within the proximal constitutive heterochromatin can undergo polytenization, contributing to the formation of β-heterochromatin.
Identified in a genetic screen for modifiers of the phl::tor12D.sev rough eye mutant phenotype.
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.
By comparing methylation by Ecol\dam methylase between euchromatic and heterochromatic genes it was determined that the heterochromatic state does not prevent methylase accessibility in vivo.
Tyrosine phosphorylation of rl and Erk-B increases during heat shock. MAP kinase activation is an immediate early response to heat shock and the increased activity is maintained throughout heat shock treatment.
Phosphorylation of aop by rl map kinase affects the stability and subcellular localisation of aop resulting in rapid down regulation of aop activity. Map kinase mediated down regulation of aop function appears to be critical for the proper differentiation of both neuronal and nonneuronal tissues throughout development. This suggests that aop is an essential component of a general timing mechanism controlling the competence of a cell to respond to inductive signals.
"h38R--h46 (determined by in situ hybridisation)" was stated as revision.
In contrast to the euchromatic genes, the heterochromatic genes, including the α-heterochromatic rl gene, require proximity to heterochromatin to function properly.
Lethal phenotype of mutations at rl have reduced and malformed wings, legs and halteres due to cell death.