Interaction Between Eye Pigment Genes and Tau-Induced Neurodegeneration in Drosophila melanogaster
Open accessAbstract
Null mutations in the genes white and brown, but not scarlet, enhance a rough eye phenotype in a Drosophila melanogaster model of tauopathy; however, adding rosy mutations suppresses these effects. Interaction with nucleotide-derived pigments or increased lysosomal dysregulation are potential mechanisms. Finally, tau toxicity correlates with increased GSK-3β activity, but not with tau phosphorylation at Ser202/Thr205.
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white and brown mutants show a strong decrease in GSK-3β activity, and a rosy mutant shows a strong increase.
“Interestingly, we also observe a strong decrease in GSK-3β activity in white and brown mutants and a strong increased activity in a rosy mutant (61).”
From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [61]
The Results passage on GSK-3β activation and Figure 4B (page not provided in our copy) say the opposite for white and white-plus-brown flies: inhibitory Ser9 phosphorylation decreases, indicating increased GSK-3β activity. Figure 4B says a rosy mutation restores that inhibitory phosphorylation in this background, not that rosy increases activity. (LLM, conf=0.92)
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Experimental — accuracy not yet measuredBackground genes white, brown and rosy were also identified as modifiers, yielding a total of 40 modifier genes.
“Additionally, in the process of conducting this screen, the background genes white, brown and rosy were also identified as modifiers (61), yielding a total of 40 modifier genes.”
From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [61]
The Abstract (page not supplied) reports that white, brown, and rosy affect the tau-induced eye phenotype, supporting their identification as modifiers. Our copy does not say they were identified during the cited screen or give a total of 40 modifier genes. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMutations in the pigment-associated genes white, brown and rosy enhance tau toxicity.
“Furthermore, we previously identified mutations in the pigment-associated genes white, brown and rosy that enhance tau toxicity (61).”
From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [61]
The Abstract says null mutations in white and brown enhance the rough-eye phenotype in the Drosophila tauopathy model. It says the opposite for rosy: adding rosy mutations suppresses those effects, rather than enhancing tau toxicity. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe w+ marker gene in the P elements used in the P lethal and EY collections modifies the tau phenotype in a w+ dose-dependent manner.
“the w+ marker gene in the P elements used in the P lethal and EY collections modified the tau phenotype in a w+ dose-dependent manner (61)”
From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [61]
Our copy (section labeled Abstract; no page available) reports that P-element insertions affected the tau rough-eye phenotype and that increasing copies of mini-white suppressed white mutation-induced toxicity in a dose-dependent manner. It does not identify the P lethal or EY collections, so the claim's collection-specific attribution is not established. (LLM, conf=0.83)
Experimental — accuracy not yet measuredGenes white, brown and rosy were identified as modifiers independent of the collections screened.
“We incorporated genes white, brown and rosy into the network, which we identified as modifiers independent of the collections we screened (61).”
From Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (2011) · cites this paper as [61]
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Cites
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Tau Phosphorylation Sites Work in Concert to Promote Neurotoxicity In Vivo
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Tau protein binds to pericentromeric DNA: a putative role for nuclear tau in nucleolar organization
Sjöberg, M. K., Shestakova, E., Mansuroglu, Z., Maccioni, R. B., & Bonnefoy, E. (2006) · Journal of Cell Science · doi:10.1242/jcs.02907 · Cited by 166 · see citing works
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Flagged first, then by citations
Research works printed but not linked: 4
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- Ohmi, K., L. C. Kudo, S. Ryazantsev, H. Z. Zhao, S. L. Karsten et al., 2009 Sanfilippo syndrome type B, a lysosomal storage disease, is also a tauopathy. Proc. Natl. Acad. Sci. USA 106: 8332-8337.
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Cited by
Sorted by citations
Ambegaokar, S. S., & Jackson, G. R. (2011) · Human Molecular Genetics · doi:10.1093/hmg/ddr432 · Cited by 113 · see citing works
“In addition, white and rosy, two modifiers of tau toxicity identified earlier from this study (61), also are important in lipid trafficking.”
BackgroundResultInfluentialSelf-citation
- Authors
- Ambegaokar, S. S., & Jackson, G. R.
- Affiliations
- University of California, Los Angeles (US)
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Jackson, George R
- Venue
- Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-09-01
- Volume
- 186
- Issue
- 1
- Pages
- 435-442
- ISSN
- 0016-6731 (ISSN-L)
- 1943-2631
- PMC
- PMC2940309
- OpenAlex
- W2105595108
- Cited by
- 30
- References
- 6
- Citations by year
- 2025: 2 · 2023: 3 · 2022: 2 · 2020: 1 · 2019: 1 · 2018: 5 · 2017: 3 · 2015: 4 · 2014: 2 · 2013: 2 · 2012: 3
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Genetics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Health Assistance Foundation
- National Institute on Aging (P50AG016570, AG 16570)
- National Institute of Mental Health (T32MH073526)
- National Institute of Neurological Disorders and Stroke (R01NS046489, NS04648)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- tauopathy, white gene, rough eye phenotype, genetic interactions, tau phosphorylation, Drosophila melanogaster
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Animals, Drosophila melanogaster, Eye, Mutation, Phenotype, Phosphorylation, Pigmentation, tau Proteins, Neurodegenerative Diseases, Drosophila Proteins, Glycogen Synthase Kinase 3
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