FB2026_03 , released September 17, 2026
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Citation
Song, Z., McCall, K., Steller, H. (1997). DCP-1, a Drosophila cell death protease essential for development.  Science 275(5299): 536--540.
FlyBase ID
FBrf0092688
Publication Type
Research paper
Abstract
Apoptosis, a form of cellular suicide, involves the activation of CED-3-related cysteine proteases (caspases). The regulation of caspases by apoptotic signals and the precise mechanism by which they kill the cell remain unknown. In Drosophila, different death-inducing stimuli induce the expression of the apoptotic activator reaper. Cell killing by reaper and two genetically linked apoptotic activators, hid and grim, requires caspase activity. A Drosophila caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be structurally and biochemically similar to Caenorhabditis elegans CED-3. Loss of zygotic DCP-1 function in Drosophila caused larval lethality and melanotic tumors, showing that this gene is essential for normal development.
PubMed ID
PubMed Central ID
Related Publication(s)
Erratum

Correction to Song et al. , Science 275 (5299) 536-540 and McCall and Steller, Science 279 (5348) 230-234.
McCall, 2004, Science 303(5661): 1138 [FBrf0225560]

Associated Information
Comments

A subsequent study (FBrf0167648) and an erratum (FBrf0225560) state that "Several phenotypes that were previously attributed to loss of 'Dcp-1', including melanotic tumors, small imaginal discs, and dumpless egg chambers, have now been shown to be due to disruption of 'pita'. However, single mutations in 'Dcp-1' show defective germline cell death, and loss of 'Dcp-1' contributes to the ovary phenotype previously reported for the P-element alleles. Thus, the original ovary phenotype reported for the P-element alleles was due to the combined loss 'Dcp-1' and 'pita'."

Associated Files
Other Information
Secondary IDs
  • FBrf0092868
Language of Publication
English
Additional Languages of Abstract
Parent Publication
Publication Type
Journal
Abbreviation
Science
Title
Science
Publication Year
1895-
ISBN/ISSN
0036-8075 1095-9203
Data From Reference
Aberrations (3)
Alleles (2)
Genes (2)
Insertions (2)