ArticlePLoS genetics2015
Pelle Modulates dFoxO-Mediated Cell Death in Drosophila.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
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- Myc suppresses male-male courtship in Drosophila.The EMBO journal · 2022Article
- Toll-7 promotes tumour growth and invasion in Drosophila.Cell proliferation · 2022Article
- Sanghuang Tongxie Formula Ameliorates Insulin Resistance inFrontiers in pharmacology · 2022Article
- The Emerging Roles of Pellino Family in Pattern Recognition Receptor Signaling.Frontiers in immunology · 2022Review
- Field cricket genome reveals the footprint of recent, abrupt adaptation in the wild.Evolution letters · 2020Article
- Toll signaling promotes JNK-dependent apoptosis inCell division · 2020Article
- Lic regulates JNK-mediated cell death in Drosophila.Cell proliferation · 2019Article
- The Toll Pathway in the Central Nervous System of Flies and Mammals.Neuromolecular medicine · 2018Review
- Three-tier regulation of cell number plasticity by neurotrophins and Tolls inThe Journal of cell biology · 2017Article
- dFoxO promotes Wingless signaling in Drosophila.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-1 receptor-associated kinases (IRAKs) are crucial mediators of the IL-1R/TLR signaling pathways that regulate the immune and inflammation response in mammals. Recent studies also suggest a critical role of IRAKs in tumor development, though the underlying mechanism remains elusive. Pelle is the sole Drosophila IRAK homolog implicated in the conserved Toll pathway that regulates Dorsal/Ventral patterning, innate immune response, muscle development and axon guidance. Here we report a novel function of pll in modulating apoptotic cell death, which is independent of the Toll pathway. We found that loss of pll results in reduced size in wing tissue, which is caused by a reduction in cell number but not cell size. Depletion of pll up-regulates the transcription of pro-apoptotic genes, and triggers caspase activation and cell death. The transcription factor dFoxO is required for loss-of-pll induced cell death. Furthermore, loss of pll activates dFoxO, promotes its translocation from cytoplasm to nucleus, and up-regulates the transcription of its target gene Thor/4E-BP. Finally, Pll physically interacts with dFoxO and phosphorylates dFoxO directly. This study not only identifies a previously unknown physiological function of pll in cell death, but also shed light on the mechanism of IRAKs in cell survival/death during tumorigenesis.
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