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This report addresses Toll-7, encoded by gene CG8595 (FlyBase: FBgn0034476, UniProt: Q7KIN0) in Drosophila melanogaster (fruit fly). Toll-7 belongs to the Toll-like receptor family and contains leucine-rich repeat domains, consistent with the UniProt annotation (kojour2023innateimmuneresponse pages 1-2, umetsu2022cellmechanicsand pages 1-3). The gene identity has been confirmed across multiple recent authoritative studies published in 2022-2024.
Toll-7 is a type I transmembrane receptor with a modular architecture consisting of three principal domains: an extracellular leucine-rich repeat (LRR) region flanked by cysteine-rich modules, a single-pass transmembrane segment, and an intracellular Toll/Interleukin-1 receptor (TIR) domain (kojour2023innateimmuneresponse pages 1-2, umetsu2022cellmechanicsand pages 1-3, lima2021evolutionoftoll pages 1-2). This architecture positions the LRR ectodomain on the cell surface for ligand recognition and cell-cell interactions, while the cytoplasmic TIR domain enables intracellular signal transduction. The receptor is localized to the plasma membrane and functions at the cell surface for ligand binding and recognition, with likely endocytosis for signaling as typical of Toll receptors (zhang2024maintainingtollsignaling pages 2-3).
Toll-7 functions as a receptor for multiple Spätzle-family cytokines, displaying promiscuous ligand binding. The receptor can bind Spätzle-1 (Spz-1), Spätzle-2/Drosophila neurotrophin-1 (Spz-2/DNT-1), and Spätzle-5/Drosophila neurotrophin-2 (Spz-5/DNT-2) (zhang2024maintainingtollsignaling pages 2-3). These ligands function as neurotrophin-like molecules in Drosophila, mediating neuronal survival, circuit connectivity, and structural synaptic plasticity (zhang2024maintainingtollsignaling pages 2-3). However, ligand-receptor relationships are context-dependent; while DNT-2 can bind Toll-7, recent studies show that specific DNT-2 developmental functions are mediated primarily through Toll-2 in the visual system and Toll-6 in dopaminergic circuits (alshamsi2025theneurotrophindnt2 pages 1-4, alshamsi2025theneurotrophindnt2 pages 14-17, alshamsi2025theneurotrophindnt2 pages 8-11).
Toll-7 employs distinct signaling pathways depending on cellular context, representing a critical difference from canonical Toll-1 signaling:
MyD88-Independent Autophagy Pathway: For autophagy regulation, Toll-7 signals through a MyD88-independent mechanism that nevertheless requires Tube, Pelle, and protein phosphatase 2A (PP2A). This pathway regulates the Akt-Tor-S6K axis, decreasing Akt phosphorylation and promoting autophagy through increased Atg8a/LC3 lipidation and reduced P62/Ref(2)P accumulation (zhang2024maintainingtollsignaling pages 3-6, zhang2024maintainingtollsignaling pages 2-3, zhang2024maintainingtollsignaling pages 6-8). Importantly, RNAi knockdown of dMyd88 suppressed Toll-1-mediated but not Toll-7-mediated autophagy-associated gene expression, demonstrating pathway divergence (zhang2024maintainingtollsignaling pages 3-6, zhang2024maintainingtollsignaling pages 1-2).
MyD88-Dependent Immune Transcription: For antimicrobial peptide production, Toll-7 engages a MyD88-dependent pathway. Overexpression of Toll-7's intracellular TIR domain (TIR-7) activated the drosomycin (Drs) antimicrobial peptide promoter, and this activation was blocked by dMyd88 knockdown (zhang2024maintainingtollsignaling pages 3-6). This likely involves the canonical Toll pathway components including Tube, Pelle, Cactus degradation, and NF-κB transcription factors Dif/Dorsal (lima2021evolutionoftoll pages 1-2, zhang2024maintainingtollsignaling pages 2-3).
TIR-Independent Cell Recognition: In olfactory system development, Toll-7 functions primarily through its extracellular domain for cell-cell recognition, independently of intracellular TIR domain signaling. The extracellular domain is sufficient for neuronal wiring specificity, suggesting Toll-7 acts as a cell-surface recognition molecule or adhesion receptor in this context (umetsu2022cellmechanicsand pages 10-12).
The most robustly characterized function of Toll-7 is the maintenance of basal autophagy in the adult Drosophila brain. Recent experimental evidence from Zhang et al. (2024) demonstrates this role through complementary approaches (zhang2024maintainingtollsignaling pages 10-12, zhang2024maintainingtollsignaling pages 8-10, zhang2024maintainingtollsignaling pages 6-8, zhang2024maintainingtollsignaling pages 2-3, zhang2024maintainingtollsignaling pages 1-2, zhang2024maintainingtollsignaling pages 3-6):
Loss-of-function studies: Toll-7 mutant flies (Toll-7^g1-5/Df(2R)) showed markedly reduced or nearly absent mCherry-Atg8a puncta and lacked detectable endogenous Atg8a-II compared with wild-type controls, indicating severely impaired autophagy (zhang2024maintainingtollsignaling pages 3-6). These mutants also exhibited altered phosphorylation of Akt, Tor, and S6K, increased accumulation of P62/Ref(2)P aggregates and ubiquitinated proteins, demonstrating defective autophagic clearance and proteostasis (zhang2024maintainingtollsignaling pages 10-12, zhang2024maintainingtollsignaling pages 3-6).
Gain-of-function studies: In Drosophila S2 cells, overexpression of Toll-7, its intracellular TIR-7 domain, or activation with Spätzle proteins increased LC3-II/LC3-PE levels (a marker of autophagosome formation), reduced P62 levels (indicating enhanced autophagic flux), and produced autophagic puncta (zhang2024maintainingtollsignaling pages 2-3, zhang2024maintainingtollsignaling pages 6-8).
Genetic epistasis: The autophagy response required Tube, Pelle, and PP2A activity; RNAi knockdown of these genes suppressed Toll-7-induced autophagy (zhang2024maintainingtollsignaling pages 10-12, zhang2024maintainingtollsignaling pages 6-8). PP2A activity was specifically increased by Toll-7 signaling (zhang2024maintainingtollsignaling pages 10-12).
Toll-7-mediated autophagy is functionally critical for dopaminergic (DA) neuron survival in the adult brain. Toll-7 loss-of-function flies showed significantly fewer tyrosine hydroxylase (TH)-positive dopaminergic neurons compared with controls and exhibited increased TUNEL staining, indicating elevated apoptosis (zhang2024maintainingtollsignaling pages 10-12, zhang2024maintainingtollsignaling pages 8-10). This neuronal loss had behavioral consequences: only approximately 70% of Toll-7 mutant flies crossed the climbing assay threshold within two minutes compared with nearly 100% of control flies, demonstrating impaired locomotor function (zhang2024maintainingtollsignaling pages 8-10). Atg8a mutants, defective in autophagy, showed comparable reductions in DA neurons and climbing ability, supporting the conclusion that autophagy is the critical mechanism linking Toll-7 to neuronal maintenance (zhang2024maintainingtollsignaling pages 10-12, zhang2024maintainingtollsignaling pages 8-10).
Spätzle-5 (Spz-5) is a candidate physiological ligand for this function, as Spz-5 mutants—but not Spz-1 mutants—showed significant dopamine neuron loss (zhang2024maintainingtollsignaling pages 10-12).
Toll-7 plays a specialized role in establishing precise connectivity in the olfactory system. It is expressed in a subset of olfactory receptor neurons (ORNs) in the antenna, where it promotes accurate axon targeting to ensure proper matching with corresponding projection neurons (PNs) in antennal-lobe glomeruli (umetsu2022cellmechanicsand pages 10-12). This function is mechanistically distinct from other Toll-7 activities: the extracellular LRR domain is sufficient for wiring specificity, while the intracellular TIR domain is dispensable (umetsu2022cellmechanicsand pages 10-12). This indicates that Toll-7 acts primarily as a cell-surface recognition tag or adhesion molecule rather than through canonical intracellular signal transduction in this developmental context.
Toll-7 and Toll-6 have complementary but distinct roles in olfactory circuit assembly, with Toll-6 acting mainly in PN dendrite targeting while Toll-7 functions in ORN axon targeting (umetsu2022cellmechanicsand pages 10-12). Importantly, the known neurotrophin ligands DNT-1 and DNT-2 are dispensable for this ORN-PN matching function, and Toll-6 and Toll-7 do not bind each other, suggesting an unidentified heterophilic cell-surface partner mediates the wiring specificity (umetsu2022cellmechanicsand pages 10-12).
Antimicrobial peptide production: Toll-7 can activate transcription of antimicrobial peptide genes, particularly drosomycin (Drs), an antifungal peptide. In S2 cells, Toll-7 and Toll-7-Spätzle complexes stimulated drosomycin promoter activity through a MyD88-dependent mechanism (zhang2024maintainingtollsignaling pages 3-6, zhang2024maintainingtollsignaling pages 2-3). This immune transcription response is mechanistically separable from Toll-7's autophagy function: dMyd88 knockdown suppressed Drs induction but did not block Toll-7-mediated Atg8a and InR expression (zhang2024maintainingtollsignaling pages 3-6).
Antiviral defense: Toll-7's role in antiviral immunity remains controversial. Earlier work proposed that Toll-7 recognizes viruses and activates antiviral autophagy (prince2023elucidatingtherole pages 15-15), but multiple recent authoritative reviews explicitly note that Toll-7's involvement in the response to viral infection remains unresolved and should not be treated as established functional annotation (umetsu2022cellmechanicsand pages 1-3). Further experimental validation is needed to clarify this potential function.
Toll-7 is a plasma membrane protein with its extracellular LRR domain exposed on the cell surface and its intracellular TIR domain in the cytoplasm (kojour2023innateimmuneresponse pages 1-2, umetsu2022cellmechanicsand pages 1-3). The receptor is highly expressed in the adult Drosophila brain, particularly in distinct anatomical domains and neuronal populations (zhang2024maintainingtollsignaling pages 2-3). Specific expression sites include:
The receptor functions at the plasma membrane for ligand binding and cell-cell recognition, and likely undergoes endocytosis for intracellular signaling, as is typical for Toll family receptors.
Toll-7 belongs to the TOLL2_7 subfamily along with Toll-2/18-wheeler, representing a lineage that arose through duplication in ancestral Diptera or Schizophora (lima2021evolutionoftoll pages 14-15, lima2021evolutionoftoll pages 8-10). This subfamily shows substantial lineage-specific expansion and gene gain/loss events, particularly in Diptera and Lepidoptera, contrasting with the more evolutionarily conserved Toll-6 and Toll-8 subfamilies (lima2021evolutionoftoll pages 14-15).
Phylogenomic analyses reveal that TOLL2_7 genes have undergone repeated duplication, neofunctionalization, and subfunctionalization, explaining their participation in diverse biological responses (lima2021evolutionoftoll pages 14-15, lima2021evolutionoftoll pages 8-10, lima2021evolutionoftoll pages 13-14). Importantly, comparative studies emphasize that homology-based functional inference may be unreliable for Toll-7; its functions cannot be safely extrapolated from Toll-1, other Drosophila Toll receptors, or vertebrate TLRs despite structural similarities (lima2021evolutionoftoll pages 8-10).
This evolutionary context helps explain Toll-7's functional diversity: the receptor combines ancestral immune-related functions with derived developmental and neuronal roles that emerged through gene duplication and divergence (lima2021evolutionoftoll pages 14-15, lima2021evolutionoftoll pages 13-14).
| Function/process | Molecular mechanism | Ligands/partners | Tissue/localization | Key evidence |
|---|---|---|---|---|
| Basal autophagy and proteostasis | Cell-surface Toll-7 activates a MyD88-independent but Tube–Pelle–PP2A-dependent pathway. Signaling lowers Akt activity and modulates the Akt–Tor–S6K axis, increases Atg8a-associated autophagy, and promotes clearance of Ref(2)P/P62 and ubiquitinated proteins. The adaptor connecting Toll-7 to Tube/Pelle remains unresolved. | Active Spätzle proteins; biochemical interaction or activity has been reported with Spz-1, Spz-2/DNT-1, and Spz-5/DNT-2. Tube, Pelle, PP2A, Akt, Tor, S6K, Atg8a, and Ref(2)P/P62 are downstream components or readouts. | Adult brain and cultured Drosophila S2 cells; receptor signaling begins at the plasma membrane, with downstream effects on cytoplasmic autophagy machinery. | Toll-7/TIR-7 gain-of-function increased LC3-II/Atg8a-II and autolysosomal puncta and reduced P62 in S2 cells. Toll-7 mutants had nearly absent mCherry-Atg8a puncta and Atg8a-II, altered Akt/Tor/S6K phosphorylation, and accumulated P62 and ubiquitinated proteins. RNAi epistasis showed dependence on Tube, Pelle, and PP2A but not MyD88 for autophagy-associated outputs (zhang2024maintainingtollsignaling pages 3-6, zhang2024maintainingtollsignaling pages 6-8, zhang2024maintainingtollsignaling pages 2-3). |
| Dopaminergic-neuron survival and locomotor maintenance | Toll-7-dependent basal autophagy maintains neuronal proteostasis; impaired signaling is associated with aggregate accumulation, apoptosis, dopaminergic-neuron loss, and motor dysfunction. The data strongly associate autophagy failure with neuron loss, although rescue by Atg1 or rapamycin was not tested, limiting proof of direct causality. | Spz-5 is a candidate physiological ligand because Spz-5 mutants—but not Spz-1 mutants—showed dopaminergic-neuron loss. Atg8a provides a genetic/phenotypic comparator. | Adult brain, including TH-positive dopaminergic neurons. | Toll-7 loss-of-function and brain-specific RNAi reduced TH-positive neuron number and increased TUNEL staining. About 70% of Toll-7 mutants crossed the climbing threshold within two minutes versus nearly 100% of controls; Atg8a mutants showed comparable neuronal and behavioral defects (zhang2024maintainingtollsignaling pages 10-12, zhang2024maintainingtollsignaling pages 8-10, zhang2024maintainingtollsignaling pages 6-8). |
| Olfactory-circuit wiring and partner matching | Toll-7 acts principally as an extracellular cell-recognition/tagging receptor rather than through canonical TIR-domain signaling. Its extracellular domain is sufficient for wiring specificity; the intracellular domain is dispensable. | Unknown heterophilic cell-surface partner. Toll-6 and Toll-7 do not bind each other; DNT-1 and DNT-2 are dispensable for this particular matching function. | Cell surface of a subset of olfactory receptor neurons; Toll-7 guides ORN axons toward appropriate projection-neuron partners in antennal-lobe glomeruli. | Genetic/domain-manipulation studies showed defects in ORN axon targeting and ORN–PN matching and demonstrated sufficiency of the Toll-7 extracellular region. Toll-6 has a complementary role, acting mainly in PN dendrite targeting (umetsu2022cellmechanicsand pages 10-12). |
| Neurotrophin-like signaling, neuronal survival, and connectivity | Toll-7 can serve as a receptor for Spätzle-family neurotrophin-like ligands and has been associated with neuronal survival, connectivity, and structural synaptic plasticity. Ligand–receptor usage is promiscuous and context dependent; not every DNT-2 phenotype is mediated by Toll-7. | Strongest prior assignment: Spz-2/DNT-1–Toll-7. Spz-5/DNT-2 can also bind Toll-7, but DNT-2 prominently signals through Toll-6/Kek-6 in dopaminergic circuits and through Toll-2 in the developing visual system. | Distinct neuronal domains in the developing and adult brain; exact Toll-7-positive populations vary by circuit. | Binding and receptor-activation studies support interactions with Spz-2 and Spz-5. Recent work confirms DNT receptor promiscuity but attributes specific dopaminergic and visual-system DNT-2 phenotypes chiefly to Toll-6 or Toll-2, so Toll-7-specific in-vivo causality remains less secure (zhang2024maintainingtollsignaling pages 2-3, alshamsi2025theneurotrophindnt2 pages 1-4, alshamsi2025theneurotrophindnt2 pages 14-17, alshamsi2025theneurotrophindnt2 pages 8-11). |
| Antimicrobial transcription | Toll-7 can engage a MyD88-dependent immune-transcription branch: TIR-7 activates the drosomycin promoter, and MyD88 knockdown suppresses this response. This differs from Toll-7-induced autophagy, which is MyD88 independent. Canonical downstream NF-κB factors are plausible, but their Toll-7-specific requirement was not established in the cited experiments. | MyD88; likely canonical Toll-pathway components Tube, Pelle, Cactus, Dif/Dorsal. Tested extracellular partners include Spz-1, Spz-2, and Spz-5. | Demonstrated primarily in Drosophila S2 cells; systemic physiological relevance and tissue of action remain incompletely defined. | TIR-7 overexpression and Toll-7–Spätzle combinations activated drosomycin (Drs) reporter/expression. MyD88 RNAi inhibited Drs induction but did not inhibit Toll-7-mediated Atg8a/InR responses, experimentally separating immune transcription from autophagy signaling (zhang2024maintainingtollsignaling pages 3-6, zhang2024maintainingtollsignaling pages 2-3). |
| Antiviral recognition/autophagy—contested assignment | A 2012 study proposed direct viral recognition by Toll-7 followed by antiviral autophagy. Subsequent reviews emphasize that Toll-7’s antiviral role remains controversial, so it should not be treated as settled functional annotation. | Vesicular stomatitis virus was reported as the viral stimulus or binding target; the downstream mechanism was described as noncanonical antiviral autophagy. | Proposed at the surface and intracellular signaling machinery of virus-exposed Drosophila cells and tissues. | Earlier infection experiments linked Toll-7 to virus recognition and antiviral autophagy, but later expert reviews explicitly characterize the assignment as unresolved. Evidence for generalized antiviral activity or broad antimicrobial-peptide control is insufficient (umetsu2022cellmechanicsand pages 1-3, lima2021evolutionoftoll pages 13-14, prince2023elucidatingtherole pages 15-15). |
| Receptor architecture enabling signaling and recognition | Predicted/annotated type-I single-pass transmembrane receptor: N-terminal extracellular leucine-rich repeats with cysteine-rich flanking modules, one transmembrane helix, and a cytoplasmic TIR domain. This topology supports extracellular ligand/cell recognition and intracellular signal initiation; no Toll-7-specific experimental atomic structure was identified. | Extracellular Spätzle-family ligands or unidentified cell-surface partners; cytoplasmic signaling factors interact functionally downstream of the TIR region. | Plasma membrane, with the LRR ectodomain outside the cell and TIR domain in the cytoplasm. | Conserved domain architecture agrees with UniProt Q7KIN0/InterPro annotations and comparative analyses of insect Toll receptors. Toll-7-specific domain boundaries and high-resolution structure remain unavailable (kojour2023innateimmuneresponse pages 1-2, umetsu2022cellmechanicsand pages 1-3, lima2021evolutionoftoll pages 1-2). |
| Evolutionary context and functional diversification | Toll-7 belongs to the TOLL2_7 subfamily with Toll-2/18-wheeler. Lineage-specific duplication, gain/loss, and possible neofunctionalization caution against assigning Toll-7 functions solely from other insect Tolls or mammalian TLRs. | Evolutionary relationship to Toll-2; function cannot safely be extrapolated from Toll-1, Toll-6, Toll-8, vertebrate TLR7, or similarly named receptors in other organisms. | Drosophila and related dipteran lineages; this is phylogenetic rather than subcellular localization evidence. | Comparative phylogenomic analysis found substantial lineage-specific expansion and placed Toll-7 in a distinct Toll2_7 evolutionary group. Authors warn that homology-based annotation is unreliable for this subfamily (lima2021evolutionoftoll pages 14-15, lima2021evolutionoftoll pages 8-10). |
Table: Summary of experimentally supported and proposed functions of Drosophila melanogaster Toll-7 (Q7KIN0), distinguishing its MyD88-dependent immune output, MyD88-independent autophagy pathway, and signaling-independent neuronal recognition role. Evidence limitations and contested assignments are explicitly noted.
Toll-7 in Drosophila melanogaster is a multifunctional receptor that coordinates neuronal homeostasis, development, and immunity through context-dependent signaling mechanisms. Its primary experimentally validated functions include:
The receptor's ability to employ distinct signaling mechanisms—MyD88-dependent versus MyD88-independent pathways, and TIR-dependent versus TIR-independent functions—represents a sophisticated regulatory strategy that allows a single receptor to coordinate multiple aspects of neuronal and immune physiology. Recent high-quality studies (2022-2024) have substantially advanced our understanding of Toll-7, particularly its critical role in autophagy and neuronal maintenance, though some proposed functions (notably antiviral defense) require further experimental validation.
Key recent publications include:
- Zhang et al. (2024). "Maintaining Toll signaling in Drosophila brain is required to sustain autophagy for dopamine neuron survival." iScience 27:108795. DOI: 10.1016/j.isci.2024.108795
- Sun et al. (2024). "A neurotrophin functioning with a Toll regulates structural plasticity in a dopaminergic circuit." eLife 13. DOI: 10.7554/elife.102222.2
- Umetsu (2022). "Cell mechanics and cell-cell recognition controls by Toll-like receptors in tissue morphogenesis and homeostasis." Fly 16:233-247. DOI: 10.1080/19336934.2022.2074783
- Lima et al. (2021). "Evolution of Toll, Spatzle and MyD88 in insects: the problem of the Diptera bias." BMC Genomics 22. DOI: 10.1186/s12864-021-07886-7
References
(kojour2023innateimmuneresponse pages 1-2): Maryam Ali Mohammadie Kojour, Ho Am Jang, Yong Seok Lee, Yong Hun Jo, and Yeon Soo Han. Innate immune response of tmtoll-3 following systemic microbial infection in tenebrio molitor. International Journal of Molecular Sciences, 24:6751, Apr 2023. URL: https://doi.org/10.3390/ijms24076751, doi:10.3390/ijms24076751. This article has 11 citations.
(umetsu2022cellmechanicsand pages 1-3): Daiki Umetsu. Cell mechanics and cell-cell recognition controls by toll-like receptors in tissue morphogenesis and homeostasis. Fly, 16:233-247, May 2022. URL: https://doi.org/10.1080/19336934.2022.2074783, doi:10.1080/19336934.2022.2074783. This article has 23 citations and is from a peer-reviewed journal.
(lima2021evolutionoftoll pages 1-2): Letícia Ferreira Lima, André Quintanilha Torres, Rodrigo Jardim, Rafael Dias Mesquita, and Renata Schama. Evolution of toll, spatzle and myd88 in insects: the problem of the diptera bias. BMC Genomics, Jul 2021. URL: https://doi.org/10.1186/s12864-021-07886-7, doi:10.1186/s12864-021-07886-7. This article has 39 citations and is from a peer-reviewed journal.
(zhang2024maintainingtollsignaling pages 2-3): Jie Zhang, Ting Tang, Ruonan Zhang, Liang Wen, Xiaojuan Deng, Xiaoxia Xu, Wanying Yang, Fengliang Jin, Yang Cao, Yuzhen Lu, and Xiao-Qiang Yu. Maintaining toll signaling in drosophila brain is required to sustain autophagy for dopamine neuron survival. iScience, 27:108795, Feb 2024. URL: https://doi.org/10.1016/j.isci.2024.108795, doi:10.1016/j.isci.2024.108795. This article has 15 citations and is from a peer-reviewed journal.
(alshamsi2025theneurotrophindnt2 pages 1-4): Naser Alshamsi, Francisca Rojo-Cortés, Bangfu Zhu, Samaher Fahy, Guiyi Li, Anna Lassota, Marta Moreira, and Alicia Hidalgo. The neurotrophin dnt-2 regulates cell survival and connectivity via the toll-2 receptor during visual system development of drosophila. BioRxiv, Jul 2025. URL: https://doi.org/10.1101/2025.07.18.665476, doi:10.1101/2025.07.18.665476. This article has 0 citations.
(alshamsi2025theneurotrophindnt2 pages 14-17): Naser Alshamsi, Francisca Rojo-Cortés, Bangfu Zhu, Samaher Fahy, Guiyi Li, Anna Lassota, Marta Moreira, and Alicia Hidalgo. The neurotrophin dnt-2 regulates cell survival and connectivity via the toll-2 receptor during visual system development of drosophila. BioRxiv, Jul 2025. URL: https://doi.org/10.1101/2025.07.18.665476, doi:10.1101/2025.07.18.665476. This article has 0 citations.
(alshamsi2025theneurotrophindnt2 pages 8-11): Naser Alshamsi, Francisca Rojo-Cortés, Bangfu Zhu, Samaher Fahy, Guiyi Li, Anna Lassota, Marta Moreira, and Alicia Hidalgo. The neurotrophin dnt-2 regulates cell survival and connectivity via the toll-2 receptor during visual system development of drosophila. BioRxiv, Jul 2025. URL: https://doi.org/10.1101/2025.07.18.665476, doi:10.1101/2025.07.18.665476. This article has 0 citations.
(zhang2024maintainingtollsignaling pages 3-6): Jie Zhang, Ting Tang, Ruonan Zhang, Liang Wen, Xiaojuan Deng, Xiaoxia Xu, Wanying Yang, Fengliang Jin, Yang Cao, Yuzhen Lu, and Xiao-Qiang Yu. Maintaining toll signaling in drosophila brain is required to sustain autophagy for dopamine neuron survival. iScience, 27:108795, Feb 2024. URL: https://doi.org/10.1016/j.isci.2024.108795, doi:10.1016/j.isci.2024.108795. This article has 15 citations and is from a peer-reviewed journal.
(zhang2024maintainingtollsignaling pages 6-8): Jie Zhang, Ting Tang, Ruonan Zhang, Liang Wen, Xiaojuan Deng, Xiaoxia Xu, Wanying Yang, Fengliang Jin, Yang Cao, Yuzhen Lu, and Xiao-Qiang Yu. Maintaining toll signaling in drosophila brain is required to sustain autophagy for dopamine neuron survival. iScience, 27:108795, Feb 2024. URL: https://doi.org/10.1016/j.isci.2024.108795, doi:10.1016/j.isci.2024.108795. This article has 15 citations and is from a peer-reviewed journal.
(zhang2024maintainingtollsignaling pages 1-2): Jie Zhang, Ting Tang, Ruonan Zhang, Liang Wen, Xiaojuan Deng, Xiaoxia Xu, Wanying Yang, Fengliang Jin, Yang Cao, Yuzhen Lu, and Xiao-Qiang Yu. Maintaining toll signaling in drosophila brain is required to sustain autophagy for dopamine neuron survival. iScience, 27:108795, Feb 2024. URL: https://doi.org/10.1016/j.isci.2024.108795, doi:10.1016/j.isci.2024.108795. This article has 15 citations and is from a peer-reviewed journal.
(umetsu2022cellmechanicsand pages 10-12): Daiki Umetsu. Cell mechanics and cell-cell recognition controls by toll-like receptors in tissue morphogenesis and homeostasis. Fly, 16:233-247, May 2022. URL: https://doi.org/10.1080/19336934.2022.2074783, doi:10.1080/19336934.2022.2074783. This article has 23 citations and is from a peer-reviewed journal.
(zhang2024maintainingtollsignaling pages 10-12): Jie Zhang, Ting Tang, Ruonan Zhang, Liang Wen, Xiaojuan Deng, Xiaoxia Xu, Wanying Yang, Fengliang Jin, Yang Cao, Yuzhen Lu, and Xiao-Qiang Yu. Maintaining toll signaling in drosophila brain is required to sustain autophagy for dopamine neuron survival. iScience, 27:108795, Feb 2024. URL: https://doi.org/10.1016/j.isci.2024.108795, doi:10.1016/j.isci.2024.108795. This article has 15 citations and is from a peer-reviewed journal.
(zhang2024maintainingtollsignaling pages 8-10): Jie Zhang, Ting Tang, Ruonan Zhang, Liang Wen, Xiaojuan Deng, Xiaoxia Xu, Wanying Yang, Fengliang Jin, Yang Cao, Yuzhen Lu, and Xiao-Qiang Yu. Maintaining toll signaling in drosophila brain is required to sustain autophagy for dopamine neuron survival. iScience, 27:108795, Feb 2024. URL: https://doi.org/10.1016/j.isci.2024.108795, doi:10.1016/j.isci.2024.108795. This article has 15 citations and is from a peer-reviewed journal.
(prince2023elucidatingtherole pages 15-15): Brian C. Prince, Kalvin Chan, and Claudia Rückert. Elucidating the role of dsrna sensing and toll6 in antiviral responses of culex quinquefasciatus cells. Frontiers in Cellular and Infection Microbiology, Aug 2023. URL: https://doi.org/10.3389/fcimb.2023.1251204, doi:10.3389/fcimb.2023.1251204. This article has 12 citations.
(lima2021evolutionoftoll pages 14-15): Letícia Ferreira Lima, André Quintanilha Torres, Rodrigo Jardim, Rafael Dias Mesquita, and Renata Schama. Evolution of toll, spatzle and myd88 in insects: the problem of the diptera bias. BMC Genomics, Jul 2021. URL: https://doi.org/10.1186/s12864-021-07886-7, doi:10.1186/s12864-021-07886-7. This article has 39 citations and is from a peer-reviewed journal.
(lima2021evolutionoftoll pages 8-10): Letícia Ferreira Lima, André Quintanilha Torres, Rodrigo Jardim, Rafael Dias Mesquita, and Renata Schama. Evolution of toll, spatzle and myd88 in insects: the problem of the diptera bias. BMC Genomics, Jul 2021. URL: https://doi.org/10.1186/s12864-021-07886-7, doi:10.1186/s12864-021-07886-7. This article has 39 citations and is from a peer-reviewed journal.
(lima2021evolutionoftoll pages 13-14): Letícia Ferreira Lima, André Quintanilha Torres, Rodrigo Jardim, Rafael Dias Mesquita, and Renata Schama. Evolution of toll, spatzle and myd88 in insects: the problem of the diptera bias. BMC Genomics, Jul 2021. URL: https://doi.org/10.1186/s12864-021-07886-7, doi:10.1186/s12864-021-07886-7. This article has 39 citations and is from a peer-reviewed journal.