pro-apoptotic Reaper, Hid, Grim (RHG) protein - contributes to the caspase dependent apoptosis by inhibiting the anti-apoptotic Death-associated inhibitor of apoptosis 1 (Diap1) protein
Gene model reviewed during 5.46
There is only one protein coding transcript and one polypeptide associated with this gene
Interacts with Diap2 (via BIR2 domain).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\rpr using the Feature Mapper tool.
The expression of this gene along with several others is induced in salivary glands in pupae at the time of head eversion. This stage is characterized by an increase in the ecdysone titer as well as large amounts of cell death in this tissue.
rpr transcript can first be detected at embryonic stage 5, in a broad stripe in the anterior half of the embryo, and a fainter posterior stripe. By stage 6, each of these stripes has split into two narrower stripes; one of these stripes, anterior to the cephalic furrow, persists until embryonic stage 10. From embryonic stage 11, rpr is expressed in a complex and dynamic pattern.
rpr transcript is expressed in salivary glands faintly during the late larval ecdysone pulse, and strongly after the late prepupal ecdysone pulse.
In the embryo, at stage 7 rpr is expressed in one strong and one weak stripe just posterior to the cephalic forrow, and at stage 8 it is expressed just anterior to the cephalic forrow. rpr expression marks apoptotic cells throughout embryonic development.
rpr is expressed in a pattern that is very similar to the pattern of programmed cell death as determined by acridine orange staining. The onset of rpr expression typically precedes acridine orange staining by 1 to 2 hours. Double labeling experiments were used to confirm that rpr is expressed in dying cells.
GBrowse - Visual display of RNA-Seq signalsView Dmel\rpr 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: rpr anon-WO0162936.19
W is required for larval salivary gland cell death during metamorphosis and both rpr and W function in a redundant manner to direct efficient destruction of the larval salivary gland and larval midgut during metamorphosis.
Most developmental apoptosis is unaffected in rpr single mutants, but the central nervous system is enlarged due to inappropriate survival of both larval neurons and neuroblasts. Mutant males are sterile due to an inability to bend their abdomens sufficiently for copulation.
Expression of death inducers rpr and W and the repression of death inhibitor Iap2 correlates with the onset of histolysis in the larval salivary gland, suggesting that programmed cell death may be coordinated by both inductive and repressive mechanisms.
Targetted expression of W or rpr alone in the midline cells is not sufficient to induce ectopic cell death. Coexpression rapidly induces cell death that results in axon scaffold defects characteristic of mutants with abnormal midline cell development. Results suggest that rpr and W are expressed together and cooperate to induce programmed cell death during development of the central nervous system midline.
Characterisation of grim suggests the encoded apoptotic function is upstream of putative Cys proteases and grim activity parallels that of rpr and W. Because grim triggered extensive apoptosis in at least one developmental context where rpr was not sufficient, it is possible that these proteins enter a common apoptotic pathway at different sites.
Cell death activity mediated by rpr is distinct from signalling by the mammalian tumour necrosis factor receptor 1 death domain.
Expression of rpr RNA anticipates cell killing induced either by an exogenous agent (ionising radiation) or in association with congenital defects. These responses are mediated at the level of transcriptional control by upstream sequence elements. Expression of rpr is sufficient to induce apoptosis and these cell deaths can be prevented by a viral inhibitor.
Expression of rpr is both necessary and sufficient for developmental cell death. Amino acid sequence homology is observed between the cytoplasmic domains of mouse and human Fas and TNFR1, respectively, and rpr.
Programmed cell death plays a crucial role in the development of the central nervous system midline and dying midline cells are rapidly eliminated by phagocytosis. Generation of engulfment signals in cells undergoing programmed cell death is downstream of rpr gene function. Central nervous system midline and/or ventral epidermal cells provide directional cues for migrating macrophages.
rpr represents a key regulatory switch for the activation of apoptosis in response to a variety of distinct signals.