Dcp-1 is a Drosophila short-prodomain C14 effector caspase that is activated downstream of Dronc and works with DrICE to execute apoptosis in selected developmental and stress contexts. Beyond this conserved apoptotic protease role, Dcp-1 has more restricted non-core outputs in nurse-cell death and oocyte cytoplasmic dumping, starvation-induced ovarian macroautophagy through mitochondrial SesB and ATP control, Toll/NF-kappaB dampening through DIF cleavage, and Eiger-dependent neuromuscular degeneration. Dcp-1 single mutants that leave the overlapping pita gene intact are viable and complete late nurse-cell death, but fail to execute starvation-induced germline cell death in mid-oogenesis; the larval lethality first reported for the P-element allele reflects combined loss of dcp-1 and pita.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0004197 cysteine-type endopeptidase activity | IBA GO_REF:0000033 | ACCEPT | Summary: The PAINT all-caspase node correctly transfers conserved cysteine endopeptidase activity to Dcp-1. Reason: Dcp-1 is a Drosophila C14 effector caspase; direct cloning, biochemical, and genetic evidence independently support the same cysteine endopeptidase activity that the PAINT node transfers from characterized metazoan caspases. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000047947 SUPPORTS TRANSFER The metazoan caspase node supports the retained C14 catalytic activity of Dcp-1. Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0004197 cysteine-type endopeptidase activity | IDA PMID:10481910 The Drosophila caspase inhibitor DIAP1 is essential for cell... | ACCEPT | Summary: Dcp-1 is a cysteine-type endopeptidase. Reason: Although the local copy of the DIAP1 source is abstract-only, Dcp-1 is independently established as a Drosophila caspase and the row captures its core protease activity. Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0004197 cysteine-type endopeptidase activity | IDA PMID:36002459 Apoptotic caspase inhibits innate immune signaling by cleavi... | ACCEPT | Summary: Dcp-1 cleaves the fly Toll-pathway NF-kappaB factor DIF as a C14 effector caspase. Reason: The source directly tests activated fly effector caspases and shows that Dcp-1-mediated DIF degradation requires the protease-active Dcp-1 form. Supporting Evidence: PMID:36002459 Drosophila effector caspases, drICE and DCP-1, also mediated |
| GO:0004197 cysteine-type endopeptidase activity | IDA PMID:8999799 DCP-1, a Drosophila cell death protease essential for develo... | ACCEPT | Summary: Dcp-1 is a cysteine-type endopeptidase. Reason: The cloning paper identified Dcp-1 as Drosophila caspase-1 and found that it is structurally and biochemically similar to CED-3, supporting the core cysteine endopeptidase annotation. Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0004197 cysteine-type endopeptidase activity | IEA GO_REF:0000002 | ACCEPT | Summary: InterPro caspase-domain mapping correctly assigns cysteine endopeptidase activity to Dcp-1. Reason: The InterPro signatures are caspase-family domains, and direct Dcp-1 literature confirms that the fly protein has the expected C14 cysteine endopeptidase activity. Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0004197 cysteine-type endopeptidase activity | IMP PMID:9422696 Requirement for DCP-1 caspase during Drosophila oogenesis. | ACCEPT | Summary: The oogenesis mutant paper correctly treats Dcp-1 as a caspase. Reason: The original source is an oogenesis phenotype paper, but it explicitly describes dcp-1 as encoding a caspase and the activity is independently established by the Dcp-1 cloning paper. Supporting Evidence: PMID:9422696 for the dcp-1 gene, which encodes a caspase, caused female sterility by PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be |
| GO:0005515 protein binding | IPI PMID:10481910 The Drosophila caspase inhibitor DIAP1 is essential for cell... | UNDECIDED | Summary: The DIAP1 protein-binding row is plausible but unresolved from the locally available abstract. Reason: The cached source establishes that DIAP1 restrains caspase activity but does not expose the specific Dcp-1-DIAP1 physical interaction or its direction; without full text, keep this generic protein-binding assertion unresolved. Supporting Evidence: PMID:10481910 disrupting productive IAP-caspase interactions |
| GO:0005737 cytoplasm | IBA GO_REF:0000033 | ACCEPT | Summary: The cytoplasmic PAINT localization is appropriate for the conserved fly effector caspase. Reason: Dcp-1 is a soluble effector caspase that acts downstream of Dronc in apoptotic execution; the broad cytoplasm localization is compatible with both cytosolic caspase activity and the specialized mitochondrial pool described in oogenesis. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000047947 SUPPORTS TRANSFER The PAINT node transfers a general cytoplasmic location that fits short-prodomain effector caspases including Dcp-1. Supporting Evidence: PMID:16980627 both drice and dcp-1 are substrates of dronc PMID:24862573 Dcp-1 is partially localized within mitochondria |
| GO:0005759 mitochondrial matrix | IDA PMID:24862573 The Drosophila effector caspase Dcp-1 regulates mitochondria... | KEEP AS NON CORE | Summary: A specialized pro-Dcp-1 pool is protected inside mitochondria during the SesB/autophagy branch. Reason: The source fractionated cells and ovaries and used protease protection to show that pro-Dcp-1 is internalized in mitochondria, where it controls SesB stability and starvation-induced autophagic flux rather than defining the main apoptotic execution location. Supporting Evidence: PMID:24862573 Dcp-1 is partially localized within mitochondria PMID:24862573 pro-Dcp-1 interacts with SesB in a |
| GO:0005829 cytosol | ISS GO_REF:0000024 | ACCEPT | Summary: Dcp-1 has a cytosolic pool consistent with conserved effector-caspase execution. Reason: The ISS transfer from human CASP7 is directionally sound for a soluble short-prodomain effector caspase, and Dcp-1 is experimentally placed downstream of Dronc together with DrICE. Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0006508 proteolysis | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: Proteolysis is a correct but generic consequence of Dcp-1 cysteine endopeptidase activity. Reason: InterPro propagation of a broad proteolysis process is not wrong for an active caspase, but the molecular function row and the execution-phase process describe the core function more precisely. Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0006915 apoptotic process | IBA GO_REF:0000033 | MODIFY | Summary: The broad apoptotic-process PAINT row should be tightened to execution phase. Reason: The PAINT node captures inherited effector-caspase apoptosis biology, but Dcp-1 acts downstream of Dronc as an executioner rather than as an upstream signaling component. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: PANTHER:PTN000047947 SUPPORTS SOURCE BUT NOT TARGET The node supports conserved caspase apoptosis, but the propagated top-level process is a broad parent of Dcp-1 apoptotic execution. Proposed replacements: execution phase of apoptosis Supporting Evidence: PMID:16980627 developmental apoptosis in the eye disc was completely suppressed in drice/dcp-1 double mutants PMID:21120926 vCrz PCD requires both ice and dcp-1 functions |
| GO:0006915 apoptotic process | IDA PMID:8999799 DCP-1, a Drosophila cell death protease essential for develo... | MODIFY | Summary: The broad apoptotic-process row is correct but less precise than execution phase. Reason: Dcp-1 was cloned as a death protease required for development, and later genetics placed it downstream of Dronc with DrICE in the effector-caspase branch; execution phase of apoptosis is therefore the more informative descendant. Proposed replacements: execution phase of apoptosis Supporting Evidence: PMID:8999799 zygotic DCP-1 function in Drosophila caused larval lethality PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0006915 apoptotic process | IGI PMID:31409797 Characterization of TNF-induced cell death in Drosophila rev... | MODIFY | Summary: The Eiger/TNF death row should be represented as effector-caspase execution. Reason: Dcp-1 and DrICE mediate the effector-caspase arm of Eiger-induced apoptosis; the generic apoptotic-process parent should be narrowed to their direct execution role. Proposed replacements: execution phase of apoptosis Supporting Evidence: PMID:31409797 effector caspases DrICE and Dcp-1 |
| GO:0007300 ovarian nurse cell to oocyte transport | TAS PMID:10511707 An emerging blueprint for apoptosis in Drosophila. | MODIFY | Summary: The ovarian transport row should be narrowed to nurse-cell apoptosis. Reason: The primary dcp-1 phenotype includes failed nurse-cell cytoplasmic transfer, but Dcp-1 acts through the nurse-cell death machinery rather than by transporting cytoplasm itself; nurse cell apoptotic process is the direct term. Proposed replacements: nurse cell apoptotic process Supporting Evidence: PMID:9422696 inhibiting this transfer. dcp-1- nurse cells were defective in the cytoskeletal |
| GO:0007300 ovarian nurse cell to oocyte transport | TAS PMID:11139276 The fly caspases. | MODIFY | Summary: The review-derived transport row should be narrowed to nurse-cell apoptosis. Reason: The transport defect is a consequence of failed Dcp-1-dependent nurse-cell death and cytoskeletal/nuclear remodeling, so the direct GO process for this TAS row is nurse cell apoptotic process. Proposed replacements: nurse cell apoptotic process Supporting Evidence: PMID:9422696 inhibiting this transfer. dcp-1- nurse cells were defective in the cytoskeletal |
| GO:0008234 cysteine-type peptidase activity | IEA GO_REF:0000002 | MODIFY | Summary: The IEA cysteine-type peptidase row should be narrowed to the endopeptidase activity already supported for Dcp-1. Reason: Dcp-1 is not just a generic cysteine peptidase: it is a C14 caspase endopeptidase, and the existing GOA set already contains the better activity term. Proposed replacements: cysteine-type endopeptidase activity Supporting Evidence: PMID:8999799 caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be PMID:16980627 both drice and dcp-1 are substrates of dronc |
| GO:0009267 cellular response to starvation | IMP PMID:18794330 Effector caspase Dcp-1 and IAP protein Bruce regulate starva... | MODIFY | Summary: The starvation-response row should be narrowed to macroautophagy regulation. Reason: Starvation is the experimental and physiological context in this ovarian branch; the process Dcp-1 directly promotes is macroautophagic flux during mid-oogenesis. Proposed replacements: positive regulation of macroautophagy Supporting Evidence: PMID:18794330 At these two stages, the effector caspase Dcp-1 and the inhibitor |
| GO:0010508 positive regulation of autophagy | IDA PMID:20100334 A genetic screen for modifiers of Drosophila caspase Dcp-1 r... | MODIFY | Summary: The autophagy regulator row should be narrowed to macroautophagy. Reason: The genetic modifier screen uses Atg8b-GFP and Atg5 to connect Dcp-1 to the macroautophagy machinery, so the more specific macroautophagy regulation term is preferable. Proposed replacements: positive regulation of macroautophagy Supporting Evidence: PMID:20100334 positively regulates autophagy, possibly through feedback regulation. |
| GO:0010508 positive regulation of autophagy | IDA PMID:24862573 The Drosophila effector caspase Dcp-1 regulates mitochondria... | MODIFY | Summary: The mitochondrial SesB branch specifically supports positive regulation of macroautophagy. Reason: Dcp-1 promotes starvation-induced autophagic flux by nonproteolytically restraining the mitochondrial adenine nucleotide translocase SesB and ATP levels; this is macroautophagy rather than generic autophagy. Proposed replacements: positive regulation of macroautophagy Supporting Evidence: PMID:24862573 Dcp-1 promotes autophagy by negatively regulating SesB and PMID:24862573 pro-Dcp-1 interacts with SesB in a |
| GO:0010623 programmed cell death involved in cell development | IMP PMID:16980627 DRONC coordinates cell death and compensatory proliferation. | MODIFY | Summary: The developmental programmed-cell-death row should be narrowed to execution phase of apoptosis. Reason: dcp-1 mutants reduce developmental apoptosis and drice/dcp-1 double mutants essentially phenocopy upstream dronc loss, placing Dcp-1 in apoptotic execution rather than generic programmed cell death. Proposed replacements: execution phase of apoptosis Supporting Evidence: PMID:16980627 developmental apoptosis in the eye disc was completely suppressed in drice/dcp-1 double mutants PMID:21120926 vCrz PCD requires both ice and dcp-1 functions |
| GO:0012501 programmed cell death | IDA PMID:21120926 Drosophila caspases involved in developmentally regulated pr... | MODIFY | Summary: The vCrz programmed-cell-death row should be narrowed to apoptotic execution. Reason: Dcp-1 and Ice cooperate as effector caspases for the timely removal of vCrz neurons during metamorphosis; the direct role is executioner-caspase activity in apoptosis. Proposed replacements: execution phase of apoptosis Supporting Evidence: PMID:21120926 vCrz PCD requires both ice and dcp-1 functions |
| GO:0016239 positive regulation of macroautophagy | IMP PMID:18794330 Effector caspase Dcp-1 and IAP protein Bruce regulate starva... | KEEP AS NON CORE | Summary: Positive regulation of macroautophagy is a real but contextual ovarian Dcp-1 output. Reason: Dcp-1 promotes starvation-induced autophagic flux in midstage egg chambers and l(2)mbn cells, but this SesB/autophagy branch is not the core apoptotic protease role. Supporting Evidence: PMID:18794330 At these two stages, the effector caspase Dcp-1 and the inhibitor PMID:24862573 Dcp-1 promotes autophagy by negatively regulating SesB and |
| GO:0016322 neuron remodeling | IEA GO_REF:0000117 | UNDECIDED | Summary: The ARBA neuron-remodeling assertion cannot be resolved from the cached evidence. Reason: The associated primary source only exposes a statement about fly effector caspases in neurite pruning and does not name Dcp-1 in the abstract, so the automated transfer should remain undecided until the underlying full-text evidence is checked. Propagation Review Root cause: UNRESOLVED Sources checked: ARBA:ARBA00086716 SOURCE WEAK OR INFERRED The automated rule may be based on a valid full-text Dcp-1 assay, but the local abstract is not gene-specific enough to verify it. Supporting Evidence: PMID:20445064 parallel to the fly effector caspases |
| GO:0016322 neuron remodeling | IMP PMID:20445064 Axonal degeneration is regulated by the apoptotic machinery ... | UNDECIDED | Summary: The neuron-remodeling row is unresolved because the local source is abstract-only and not Dcp-1-specific. Reason: The abstract reports a role for fly effector caspases in developmental neurite pruning but does not expose whether Dcp-1 itself was perturbed, so this row cannot be manually accepted from the cached text. Supporting Evidence: PMID:20445064 parallel to the fly effector caspases |
| GO:0043025 neuronal cell body | IDA PMID:21267420 The Me31B DEAD-Box Helicase Localizes to Postsynaptic Foci a... | REMOVE | Summary: The neuronal-cell-body localization describes Drosophila decapping protein Dcp1, not caspase Dcp-1. Reason: The source uses anti-Dcp1 to mark mRNA hydrolase/P-body particles in neurons. That is the RNA decapping protein Dcp1 rather than the Dcp-1 caspase encoded by FBgn0010501. Supporting Evidence: PMID:21267420 including the mRNA hydrolases, Dcp1, and Pcm/Xrn-1 |
| GO:0043525 positive regulation of neuron apoptotic process | IBA GO_REF:0000033 | MARK AS OVER ANNOTATED | Summary: The PAINT neuron-apoptosis term is over-specific for a general fly effector caspase. Reason: Dcp-1 executes apoptosis in multiple fly tissues and can also operate in nonapoptotic autophagy or degeneration settings. The neuron-specific positive-regulation term imported from other animals overstates the supported context. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: CONTEXT OR TISSUE MISMATCH GRANULARITY MISMATCH Sources checked: PANTHER:PTN000047947 SUPPORTS SOURCE BUT NOT TARGET The all-caspase node supports Dcp-1 effector-caspase apoptosis, not a neuron-specific positive-regulation term on the fly paralog. Supporting Evidence: PMID:16980627 developmental apoptosis in the eye disc was completely suppressed in drice/dcp-1 double mutants PMID:21120926 vCrz PCD requires both ice and dcp-1 functions |
| GO:0045476 nurse cell apoptotic process | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: The ARBA nurse-cell apoptosis transfer is supported as a contextual Dcp-1 oogenesis role. Reason: Dcp-1 is repeatedly tied to nurse-cell death and nurse-cell removal during oogenesis, so the automated row is biologically sound but secondary to apoptotic execution. Propagation Review Root cause: NO FAILURE NON CORE Sources checked: ARBA:ARBA00043473 SUPPORTS TRANSFER The ARBA assertion matches the documented Dcp-1 requirement during Drosophila oogenesis. Supporting Evidence: PMID:9422696 apoptosis of the nurse cells is a necessary event for oocyte development PMID:17464325 effector caspases drice and dcp-1 also display |
| GO:0045476 nurse cell apoptotic process | IGI PMID:17464325 The Drosophila caspases Strica and Dronc function redundantl... | KEEP AS NON CORE | Summary: Dcp-1 cooperates with DrICE during developmental nurse-cell death in late oogenesis. Reason: The double-mutant genetics support redundant late-oogenesis nurse-cell roles for the two effector caspases, but the term is a tissue-specific output rather than the core execution phase. Supporting Evidence: PMID:17464325 effector caspases drice and dcp-1 also display |
| GO:0045476 nurse cell apoptotic process | IMP PMID:9422696 Requirement for DCP-1 caspase during Drosophila oogenesis. | KEEP AS NON CORE | Summary: dcp-1 mutants disrupt nurse-cell apoptosis and oocyte development. Reason: The original dcp-1 oogenesis paper directly connected the caspase to nurse-cell apoptosis and cytoskeletal/nuclear changes needed for oocyte loading; this is retained as a specialized developmental death branch. Supporting Evidence: PMID:9422696 apoptosis of the nurse cells is a necessary event for oocyte development |
| GO:0045751 negative regulation of Toll signaling pathway | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: ARBA correctly transfers Dcp-1 negative regulation of the Toll pathway through DIF cleavage. Reason: Dcp-1 can cleave and degrade DIF to repress Toll/NF-kappaB signaling, but this innate-immune damping output is a non-core substrate branch of the effector caspase. Propagation Review Root cause: NO FAILURE NON CORE Sources checked: ARBA:ARBA00084359 SUPPORTS TRANSFER The ARBA Toll-signaling term is supported by Dcp-1 cleavage of the Drosophila NF-kappaB factor DIF. Supporting Evidence: PMID:36002459 Drosophila effector caspases, drICE and DCP-1, also mediated PMID:36002459 the degradation of DIF |
| GO:0045751 negative regulation of Toll signaling pathway | IMP PMID:36002459 Apoptotic caspase inhibits innate immune signaling by cleavi... | KEEP AS NON CORE | Summary: Dcp-1 negatively regulates Toll signaling by promoting DIF degradation. Reason: Protease-active Dcp-1 represses Toll output in S2 cells through DIF cleavage and degradation; that substrate-specific immune branch is not the core apoptotic execution role. Supporting Evidence: PMID:36002459 Drosophila effector caspases, drICE and DCP-1, also mediated PMID:36002459 the degradation of DIF |
| GO:0048477 oogenesis | IMP PMID:18794330 Effector caspase Dcp-1 and IAP protein Bruce regulate starva... | MODIFY | Summary: The broad oogenesis row should be narrowed to starvation-induced macroautophagy. Reason: This source places Dcp-1 and Bruce at oogenesis nutrient-status checkpoints, where the assayed direct output is starvation-induced macroautophagy rather than oogenesis as a whole. Proposed replacements: positive regulation of macroautophagy Supporting Evidence: PMID:18794330 At these two stages, the effector caspase Dcp-1 and the inhibitor |
| GO:0048477 oogenesis | IMP PMID:24862573 The Drosophila effector caspase Dcp-1 regulates mitochondria... | MODIFY | Summary: The broad SesB/oogenesis row should be narrowed to macroautophagy regulation. Reason: The SesB paper used oogenesis to show that mitochondrial Dcp-1 controls ATP levels and autophagic flux, making positive regulation of macroautophagy a more direct term than generic oogenesis. Proposed replacements: positive regulation of macroautophagy Supporting Evidence: PMID:24862573 Dcp-1 promotes autophagy by negatively regulating SesB and PMID:24862573 pro-Dcp-1 interacts with SesB in a |
| GO:0071598 neuronal ribonucleoprotein granule | IDA PMID:17178403 Staufen- and FMRP-containing neuronal RNPs are structurally ... | REMOVE | Summary: This neuronal ribonucleoprotein granule row is a Dcp1 decapping-protein homonym error. Reason: The neuronal granule source identifies P-body RNA-degradative enzymes, including Dcp1p/DCP1, in Staufen/FMRP granules; it does not study caspase Dcp-1. Supporting Evidence: PMID:17178403 RNA-degradative enzymes Dcp1p and Xrn1p/Pacman |
| GO:0071598 neuronal ribonucleoprotein granule | IDA PMID:21267420 The Me31B DEAD-Box Helicase Localizes to Postsynaptic Foci a... | REMOVE | Summary: This second neuronal RNP row is also about Dcp1 decapping protein, not caspase Dcp-1. Reason: The Me31B paper explicitly studies the P-body mRNA hydrolase Dcp1 together with Pcm/Xrn-1 in neuronal granules, so the localization was attached to the caspase record through symbol ambiguity. Supporting Evidence: PMID:21267420 including the mRNA hydrolases, Dcp1, and Pcm/Xrn-1 |
| GO:0097194 execution phase of apoptosis | IEA GO_REF:0000117 | ACCEPT | Summary: ARBA correctly assigns apoptotic execution to Dcp-1. Reason: Dcp-1 is an effector caspase acting downstream of Dronc and redundantly with DrICE in apoptotic execution, so the execution-phase term is the correct process-level annotation. Propagation Review Root cause: NO FAILURE CORE Sources checked: ARBA:ARBA00090101 SUPPORTS TRANSFER The automated rule correctly recognizes fly Dcp-1 as an apoptotic executioner caspase. Supporting Evidence: PMID:16980627 developmental apoptosis in the eye disc was completely suppressed in drice/dcp-1 double mutants PMID:21120926 vCrz PCD requires both ice and dcp-1 functions |
| GO:0097194 execution phase of apoptosis | IMP PMID:9422696 Requirement for DCP-1 caspase during Drosophila oogenesis. | ACCEPT | Summary: Execution phase of apoptosis is the precise core process for Dcp-1. Reason: dcp-1 mutants reduce developmental apoptosis and drice/dcp-1 double mutants completely suppress apoptosis in the eye disc, placing Dcp-1 in the Dronc-to-effector execution branch. Supporting Evidence: PMID:16980627 developmental apoptosis in the eye disc was completely suppressed in drice/dcp-1 double mutants PMID:21120926 vCrz PCD requires both ice and dcp-1 functions |
| GO:1900074 negative regulation of neuromuscular synaptic transmission | IMP PMID:22153373 Glial-derived prodegenerative signaling in the Drosophila ne... | KEEP AS NON CORE | Summary: Dcp-1 is required in a prodegenerative caspase pathway at the neuromuscular junction. Reason: The Eiger/Wengen pathway engages Dark, Dronc, and Dcp-1 to drive motoneuron degeneration, with a measurable synaptic-transmission endpoint; this is a localized degeneration branch rather than canonical cell-body apoptosis. Supporting Evidence: PMID:22153373 mutations in eiger, dcp-1, debcl, and dark show no obvious NMJ phenotype |
| GO:1990525 BIR domain binding | IEA GO_REF:0000117 | UNDECIDED | Summary: The automated BIR-domain-binding assertion cannot be verified from the local abstracts. Reason: Dcp-1 likely contacts DIAP/IAP proteins, but the cached DIAP1 and DIAP2 abstracts do not expose a Dcp-1-specific BIR-domain binding assay, so the ARBA molecular-function transfer remains unresolved. Propagation Review Root cause: UNRESOLVED Sources checked: ARBA:ARBA00090447 SOURCE WEAK OR INFERRED The rule may reflect real IAP biology, but the available abstracts do not verify Dcp-1 BIR-domain binding directly. Supporting Evidence: PMID:10481910 disrupting productive IAP-caspase interactions |
| GO:1990525 BIR domain binding | IPI PMID:16485033 Systematic in vivo RNAi analysis of putative components of t... | UNDECIDED | Summary: The DIAP1 BIR-domain-binding row is plausible but not exposed by the cached source. Reason: The full text may contain the DIAP1-Dcp-1 interaction assay, but the local abstract only supports generic IAP-caspase antagonism and cannot verify BIR-domain specificity for Dcp-1. Supporting Evidence: PMID:10481910 disrupting productive IAP-caspase interactions |
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Download this section (compressed HTML)Q: The Dcp-1 P-element alleles used in early studies (for example in PMID:9422696) also disrupt the overlapping pita gene. Do the nurse-cell death and execution-phase IMP annotations from those alleles hold up with single dcp-1 mutants, given that late nurse-cell death is reported to be normal in dcp-1 single mutants (PMID:14704173)?
Q: Which endogenous Dcp-1 substrates distinguish lethal apoptotic execution from nonlethal mitochondrial SesB/autophagy and DIF/Toll signaling outputs?
Q: Does Dcp-1 bind DIAP1 through a defined BIR-domain interface in vivo, or are most BIR-domain contacts in the fly effector-caspase branch mediated by DrICE?
Q: Is Dcp-1 directly required for dendrite or axon pruning in developmental neuron remodeling, or do the neurite-pruning data support only a broader effector-caspase requirement?
Experiment: Engineer endogenous dcp-1 alleles that preserve catalytic activation but alter SesB binding, then compare apoptotic substrate cleavage, SesB abundance, ATP levels, mitochondrial morphology, and GFP-mCherry-Atg8a flux in starved midstage egg chambers.
Hypothesis: Apoptotic Dcp-1 proteolysis and the SesB-dependent macroautophagy branch use separable Dcp-1 surfaces.
Type: structure-guided endogenous separation-of-function genetics
Experiment: Run quantitative N-terminomics in matched wild-type, dcp-1-null, Drice-null, and double-mutant fly tissues undergoing eye-disc apoptosis, nurse-cell death, and vCrz neuron programmed cell death.
Hypothesis: Dcp-1 contributes to nurse-cell apoptosis, vCrz neuron apoptosis, and DrICE buffering by cleaving a substrate set distinct from the bulk DrICE execution repertoire.
Type: comparative caspase degradomics
Death caspase-1 (Dcp-1) encodes an effector caspase that cleaves specific proteins during apoptosis. It typically acts downstream of the initiator caspase encoded by Dronc. It is also involved in non-apoptotic processes such as autophagy.
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