Cited by 70Cell death mechanisms and regulationNeurobiology and Insect Physiology ResearchInvertebrate Immune Response Mechanisms

The Drosophila melanogaster Apaf-1 homologue ARK is required for most, but not all, programmed cell death

Open access
Mills, Kathryn, Daish, Tasman, Harvey, Kieran F., Pfleger, Cathie M., Hariharan, Iswar K., Kumar, Sharad·2006·The Journal of Cell Biology

Abstract

The Apaf-1 protein is essential for cytochrome c–mediated caspase-9 activation in the intrinsic mammalian pathway of apoptosis. Although Apaf-1 is the only known mammalian homologue of the Caenorhabditis elegans CED-4 protein, the deficiency of apaf-1 in cells or in mice results in a limited cell survival phenotype, suggesting that alternative mechanisms of caspase activation and apoptosis exist in mammals. In Drosophila melanogaster, the only Apaf-1/CED-4 homologue, ARK, is required for the activation of the caspase-9/CED-3–like caspase DRONC. Using specific mutants that are deficient for ark function, we demonstrate that ARK is essential for most programmed cell death (PCD) during D. melanogaster development, as well as for radiation-induced apoptosis. ark mutant embryos have extra cells, and tissues such as brain lobes and wing discs are enlarged. These tissues from ark mutant larvae lack detectable PCD. During metamorphosis, larval salivary gland removal was severely delayed in ark mutants. However, PCD occurred normally in the larval midgut, suggesting that ARK-independent cell death pathways also exist in D. melanogaster.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1083/jcb.200512126

Cites

29 of 29 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Mills, K., Daish, T., Harvey, K. F., Pfleger, C. M., Hariharan, I. K., & Kumar, S.
Affiliations
  • South Australia Pathology (AU)
  • University of California, Berkeley (US)
Corresponding author
Kumar, Sharad
Venue
The Journal of Cell Biology
Published
2006-03-13
Volume
172
Issue
6
Pages
809-815
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
OpenAlex
W2109370225
Cited by
70
References
29
Citations by year
2026: 1 · 2025: 3 · 2023: 1 · 2022: 1 · 2021: 3 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 11 · 2012: 6
FWCI
3.39
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Cell Biology (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by-nc-sa)
  • Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
  • Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc-sa)
Funders
  • National Institutes of Health
  • Medical Research Council
  • National Health and Medical Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
  • Life Sciences › Immunology and Microbiology › Immunology › Invertebrate Immune Response Mechanisms
Keywords
ark, programmed cell death, apoptosis, caspase-9 activation, Dronc, CED-4, Drosophila melanogaster, radiation-induced apoptosis, metamorphosis, salivary gland removal, larval midgut, alternative cell death pathways, developmental cell death
MeSH terms
Animals, Drosophila melanogaster, Embryo, Nonmammalian, Genes, Lethal, Larva, Metamorphosis, Biological, Mutation, Radiation, Ionizing, Salivary Glands, Signal Transduction, Apoptosis, Gene Expression Regulation, Developmental, Evolution, Molecular, Drosophila Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review