Ras, Ras1, Dras1, RasV12, dRas
ras homolog - establishes follicular cell fate during oogenesis, functions in Torso signal transduction, functions downstream EGF-R in the establishment of ventral ectoderm fate, functions downstream of Breathless in tracheal and midline glia migration, functions downstream of FGF receptor in muscle precursors and in the central nervous system, functions downstream of the EGF-R and Sevenless in differentiation in photoreceptors
Please see the JBrowse view of Dmel\Ras85D for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.41
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 5.47
2.0, 1.3 (northern blot)
1.3 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Ras85D using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: maternally deposited
JBrowse - Visual display of RNA-Seq signals
View Dmel\Ras85D in JBrowse
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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 JBrowse 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.
polyclonal
dsRNA made from templates generated with primers directed against this gene.
Ras85D plays a role in the regulation of compartment size in embryos.
dsRNA has been made from templates generated with primers directed against this gene.
Ras85D activity in the prothoracic gland regulates body size and the duration of each larval stage by regulating ecdysone release.
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 AA141103.
Ras85D controls growth, survival and differentiation in the eye. These three functions are mediated by distinct thresholds of MAPK activity.
Ras85D functions in the developing wing to regulate cellular growth.
The N-terminal portion of the cnk protein strongly cooperates with Ras85D, whereas the C-terminal portion efficiently blocks Ras85D (Ras) and phl (Raf) signalling when overexpressed in the eye. Two domains in the N-terminal portion of cnk are critical for cooperation with Ras85D. cnk functions in more than one pathway downstream of Ras85D.
Ectopic expression of activated Ras85D during imaginal disc development is sufficient to drive cell proliferation and causes hyperplastic growth of imaginal discs. Activated Ras85D induces hyperplasia of both the eye imaginal disc and the adult eye when expressed under the control of an ey enhancer fragment. In addition activated Ras85D causes non-autonomous cell death in imaginal discs and at high expression levels can lead to the complete ablation of the adult eye.
The signal promoting survival of cells in the interommatidial lattice is part of a balance between N and Ras85D pathways, which appear to act in opposition to regulate the number of interommatidial cells permitted to remain. Ras signalling promotes the 2o/3o pigment cell fate at the expense of programmed cell death in the interommatidial lattice.
Ras85D has a novel signaling function that prevents programmed cell death in the eye.
Expression of Ras85D at different times during oogenesis suggests transient Ras85D activity early in oogenesis is sufficient to cause anterior follicle cells to express posterior follicle cell markers, but is not sufficient to inhibit anterior follicle cell differentiation. Ras85D activity later in oogenesis did inhibit anterior follicle cell differentiation, antagonising the expression and activity of the slbo gene. Therefore, it appears that a sustained Ras85D signal is required first to initiate posterior follicle cell differentiation and subsequently to inhibit anterior follicle cell differentiation.
Analysis of genetic interactions among faf and R and Ras85D reveals that in addition to its critical role anterior to the morphogenetic furrow, faf has a function in undifferentiated cells alter in eye development that involves, probably indirectly, Ras85D and R. These results suggest that cells outside the facet influence cell fates within the facet.
The mechanism by which cno product controls cone cell formation in the developing compound eye is studied.
Shows no genetic interaction with sdk.
Ras85D function is required for the determination and differentiation of the midline glia.
Inactivated mutations of Ras85D enhance the P{sevhs-cswCS} phenotype.
pros gene becomes transcriptionally activated at a low level in all sev-competent cells prior to sev signaling and this requires the activities of Ras85D and two ETS transcription factors, aop and pnt. Restriction of high level pros expression to the R7 cell appears as a subsequent event, which requires sev activation of the Ras85D kinase pathway.
Loss of function alleles of Ras85D are enhancers of the cswEsev1A-3EC.sev and cswEsev1A-eOP.sev phenotype.
Ras85D is proposed to be an activator in longitudinal vein formation. There is a distinct signalling pathway activated by Egfr that interacts with Ras85D signal transduction cascade to induce crossvein formation in the wing that might be used for signalling processes elsewhere in the developing fly.
Ras CAAX peptidomimetic treatment rescues the activated Ras85D eye phenotype by suppressing the formation of supernumerary R7 cells in the compound eye. Suppression requires the CAAX element.
The phl serine/threonine kinase plays a crucial role in the R7 pathway: genetic evidence suggests that phl acts downstream of Ras85D and upstream of sina in the sev R7 signal transduction pathway.
Ras85D is required for photoreceptor development, acts in the developing R7 cell to attenuate the signalling by the sev gene product and is a suppressor of the Egfr phenotype to restore the eye to a nearly normal appearance.
The transcription pattern of Ras85D was analyzed in neuroblasts derived from tumerous larval brain of l(2)gl larvae and S2 tissue culture cells. Ras85D expresses constitutive as well as maternal/embryonic-specific transcripts.
Ras85D has been cloned and sequenced.
Codes for a polypeptide of 21.6 kilodaltons; residues 1-121 and 137-64 exhibit 75% homology with vertebrate H-ras protein.
Source for merge of: Ras85D l(3)06677
Loss-of-function mutations are homozygous lethal; enhance sev and EgfrE1 in heterozygotes (M. Simon).
