ArticleGenetics2013
The innate immune response transcription factor relish is necessary for neurodegeneration in a Drosophila model of ataxia-telangiectasia.
Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 104 citations in OpenAlex.
- Recent Advances in Therapy for the Neurodegenerative Disorder Ataxia-Telangiectasia.International journal of molecular sciences · 2026Review
- Genetic variation in innate immune gene expression influences mortality after traumatic brain injury in Drosophila.G3 (Bethesda, Md.) · 2026Article
- From retina to brain: retinal dysfunction and dopaminergic neurodegeneration inFrontiers in cell and developmental biology · 2026Article
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- Wings of Discovery: UsingCells · 2025Review
- Emerging roles of antimicrobial peptides in innate immunity, neuronal function, and neurodegeneration.Trends in neurosciences · 2024Review
- The NF-κB Factor Relish maintains blood progenitor homeostasis in the developing Drosophila lymph gland.PLoS genetics · 2024Article
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- Unraveling the intricate link between cell death and neuroinflammation usingFrontiers in cell and developmental biology · 2024Review
- Mutations in abnormal spindle disrupt temporal transcription factor expression and trigger immune responses in the Drosophila brain.Genetics · 2023Article
- Defective phagocytosis leads to neurodegeneration through systemic increased innate immune signaling.iScience · 2023Article
- Steroid hormone regulation of innate immunity in Drosophila melanogaster.PLoS genetics · 2023Review
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- Antimicrobial peptides do not directly contribute to aging in Drosophila, but improve lifespan by preventing dysbiosis.Disease models & mechanisms · 2023Article
- Unraveling the Role of Antimicrobial Peptides in Insects.International journal of molecular sciences · 2023Review
- Downregulation of oxidative stress-mediated glial innate immune response suppresses seizures in a fly epilepsy model.Cell reports · 2023Article
- Vexed mutations promote degeneration of dopaminergic neurons through excessive activation of the innate immune response.NPJ Parkinson's disease · 2022Article
- Caspar, an adapter for VAPB and TER94, modulates the progression of ALS8 by regulating IMD/NFκB-mediated glial inflammation in a Drosophila model of human disease.Human molecular genetics · 2022Article
- Eosin whole-brain mount staining to analyze neurodegeneration in a fly model of Alzheimer's disease.STAR protocols · 2022Article
- Repeated truncation of a modular antimicrobial peptide gene for neural context.PLoS genetics · 2022Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegeneration is a hallmark of the human disease ataxia-telangiectasia (A-T) that is caused by mutation of the A-T mutated (ATM) gene. We have analyzed Drosophila melanogaster ATM mutants to determine the molecular mechanisms underlying neurodegeneration in A-T. Previously, we found that ATM mutants upregulate the expression of innate immune response (IIR) genes and undergo neurodegeneration in the central nervous system. Here, we present evidence that activation of the IIR is a cause of neurodegeneration in ATM mutants. Three lines of evidence indicate that ATM mutations cause neurodegeneration by activating the Nuclear Factor-κB (NF-κB) transcription factor Relish, a key regulator of the Immune deficiency (Imd) IIR signaling pathway. First, the level of upregulation of IIR genes, including Relish target genes, was directly correlated with the level of neurodegeneration in ATM mutants. Second, Relish mutations inhibited upregulation of IIR genes and neurodegeneration in ATM mutants. Third, overexpression of constitutively active Relish in glial cells activated the IIR and caused neurodegeneration. In contrast, we found that Imd and Dif mutations did not affect neurodegeneration in ATM mutants. Imd encodes an activator of Relish in the response to gram-negative bacteria, and Dif encodes an immune responsive NF-κB transcription factor in the Toll signaling pathway. These data indicate that the signal that causes neurodegeneration in ATM mutants activates a specific NF-κB protein and does so through an unknown activator. In summary, these findings suggest that neurodegeneration in human A-T is caused by activation of a specific NF-κB protein in glial cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.