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FB2026_01
,
released March 12, 2026
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
Please see the JBrowse view of Dmel\rpr 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 5.46
1.3 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
65 (aa)
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 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: 12-14 hr APF
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.
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.
JBrowse - Visual display of RNA-Seq signals
View Dmel\rpr in JBrowse3-45
3-41.7
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 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.
New stable cell line derived from S2-unspecified : S2 cells stably expressing 3' UTRs from miRNA-targeted mRNAS attached to a Luciferase reporter were created. Two of the lines carry the hid 3' UTR with a wild type or mutated MRE (microRNA recognition element) for the miR-2 family. The other two carry the rpr 3' UTR with wild type or mutated MREs for mir-ban.
New stable cell line derived from S2-unspecified : Stable S2 cells expressing rpr under the control of the MtnA promoter (S2-Mt-reaper) were used.
rpr self-dimerisation is necessary to promote apoptotic activity.
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.
rpr can induce apoptosis in follicle cells.
rpr may participate in initiating apoptosis by stably blocking K+ channels.
Apoptosis of SL2 cells that is induced by expression of rpr can be partially prevented by expression of Cele\ced-9, Hsap\BCL2 and Hsap\BCL2L1.
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.
Glial apoptosis is blocked in embryos deficient for 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.
Source for merge of: rpr anon-WO0162936.19
Can induce or accelerate apoptosis in Xenopus egg extracts, and acts in conjunction with cytoplasmic factors to trigger mitochondrial cytochrome c release.
Source for merge of rpr anon-WO0162936.19 was sequence comparison ( date:051113 ).