Retrograde neurotrophin signaling through Tollo regulates synaptic growth in <i>Drosophila</i>

Ballard, Shannon; Miller, Daniel; Ganetzky, Barry

doi:10.1083/jcb.201308115

Cited by 47 publications

(60 citation statements)

References 80 publications

(152 reference statements)

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“…The Spz-3 signal seems to be received by the Toll-8 receptor at least in the pigmented area in the Ze and p S mutant strains. The same ligand/receptor relationship has been reported in the neuromuscular junction of D. melanogaster (27). Because our recent study has shown that the p S phenotype is controlled by the apt-like-encoding transcription factor (7), this Spz-3/Toll-8 signaling pathway likely interacts with the genetic circuit of apt-like and contributes to the phenotypic diversity of caterpillars.…”

Section: Discussionmentioning

confidence: 79%

“…An important question is whether the Bmspz-3 gene works on melanization through the Toll signaling pathway. Because Spz-3 works as a ligand of Toll-8 in neuromuscle joint formation in D. melanogaster (27), siRNA of BmToll-8 was injected into Ze and p S larva, which resulted in the loss of pigmentation patterns in both strains (red arrowheads in Fig. 4 C and D, respectively), similar to the phenotypic change observed in the Bmspz-3-knockdown larva (Figs.…”

Section: Spz-3 Work As a Putative Ligand Of Toll-8 Inmentioning

confidence: 82%

See 1 more Smart Citation

Toll ligand Spätzle3 controls melanization in the stripe pattern formation in caterpillars

Kondo

Yoda

Mizoguchi

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The authors note that two references were omitted from the article. The complete references appear below.Citations to refs. 42 and 43 should be included on page 8340, left column, second paragraph, line 23, where the reference callout "(33, 34)" should instead appear as " (33,34, 42, 43)." Also, on the same page, right column, first full paragraph, line 4, the reference callout "(36)" should instead appear as "(36, 42)." Lastly, in the same paragraph, line 9, the reference callout "(33, 34)" should instead appear as " (33,34, 42, 43)."

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Section: Discussionmentioning

confidence: 79%

Section: Spz-3 Work As a Putative Ligand Of Toll-8 Inmentioning

confidence: 82%

Toll ligand Spätzle3 controls melanization in the stripe pattern formation in caterpillars

Kondo

Yoda

Mizoguchi

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…Drosophila Toll receptors are highly expressed during embryogenesis, pointing to developmental functions (49,54). Indeed, a subset of Toll receptors, including Toll-7, function as neurotrophin receptors and are activated by members of the Spaetzle family in the developing nervous system (36,55). Drosophila Toll receptors were also recently shown to function as adhesion molecules during elongation of the antero-posterior axis of the embryo (56).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity

Lamiable

Arnold

Faria

et al. 2016

J Virol

112

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Antiviral immunity in the model organism Drosophila melanogaster involves the broadly active intrinsic mechanism of RNA interference (RNAi) and virus-specific inducible responses. Here, using a panel of six viruses, we investigated the role of hemocytes and autophagy in the control of viral infections. Injection of latex beads to saturate phagocytosis, or genetic depletion of hemocytes, resulted in decreased survival and increased viral titers following infection with Cricket paralysis virus (CrPV), Flock House virus (FHV), and vesicular stomatitis virus (VSV) but had no impact on Drosophila C virus (DCV), Sindbis virus (SINV), and Invertebrate iridescent virus 6 (IIV6) infection. In the cases of CrPV and FHV, apoptosis was induced in infected cells, which were phagocytosed by hemocytes. In contrast, VSV did not trigger any significant apoptosis but we confirmed that the autophagy gene Atg7 was required for full virus resistance, suggesting that hemocytes use autophagy to recognize the virus. However, this recognition does not depend on the Toll-7 receptor. Autophagy had no impact on DCV, CrPV, SINV, or IIV6 infection and was required for replication of the sixth virus, FHV. Even in the case of VSV, the increases in titers were modest in Atg7 mutant flies, suggesting that autophagy does not play a major role in antiviral immunity in Drosophila. Altogether, our results indicate that, while autophagy plays a minor role, phagocytosis contributes to virus-specific immune responses in insects. IMPORTANCEPhagocytosis and autophagy are two cellular processes that involve lysosomal degradation and participate in Drosophila immunity. Using a panel of RNA and DNA viruses, we have addressed the contribution of phagocytosis and autophagy in the control of viral infections in this model organism. We show that, while autophagy plays a minor role, phagocytosis contributes to virusspecific immune responses in Drosophila. This work brings to the front a novel facet of antiviral host defense in insects, which may have relevance in the control of virus transmission by vector insects or in the resistance of beneficial insects to viral pathogens.

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“…We suggest that trafficking of receptors in addition to Wit are altered in the mutants described above, and it is the altered signaling of these additional receptors that is at least partly responsible for the transmitter release phenotype. Drosophila motor nerve terminals express a cholecystokinin-like receptor (CCKLR), a toll-like receptor, a metabotropic glutamate receptor (mGluRA) and likely the insulin receptor (Ballard et al, 2014;Bogdanik et al, 2004;Chen and Ganetzky, 2012;Howlett et al, 2008). Loss of mGluRA increases evoked transmitter release (Bogdanik et al, 2004;Howlett et al, 2008), raising the possibility that increased mGluRA signaling might decrease transmitter release, which could explain the decreased transmitter release observed in these receptor trafficking mutants.…”

Section: Rtnl1 Affects Evoked Neurotransmitter Release From Multiple mentioning

confidence: 99%

The effects of ER morphology on synaptic structure and function in Drosophila melanogaster

Summerville

Faust

Fan

et al. 2016

Journal of Cell Science

108

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Hereditary spastic paraplegia (HSP) is a set of genetic diseases caused by mutations in one of 72 genes that results in age-dependent corticospinal axon degeneration accompanied by spasticity and paralysis. Two genes implicated in HSPs encode proteins that regulate endoplasmic reticulum (ER) morphology. Atlastin 1 (ATL1, also known as SPG3A) encodes an ER membrane fusion GTPase and reticulon 2 (RTN2, also known as SPG12) helps shape ER tube formation. Here, we use a new fluorescent ER marker to show that the ER within wild-type Drosophila motor nerve terminals forms a network of tubules that is fragmented and made diffuse upon loss of the atlastin 1 ortholog atl. atl or Rtnl1 loss decreases evoked transmitter release and increases arborization. Similar to other HSP proteins, Atl inhibits bone morphogenetic protein (BMP) signaling, and loss of atl causes age-dependent locomotor deficits in adults. These results demonstrate a crucial role for ER in neuronal function, and identify mechanistic links between ER morphology, neuronal function, BMP signaling and adult behavior.

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Retrograde neurotrophin signaling through Tollo regulates synaptic growth in Drosophila

Abstract: The Toll-like receptor Tollo positively regulates growth of the Drosophila larval neuromuscular junction through the JNK pathway after activation by the neurotrophin Spätzle3.

Cited by 47 publications

References 80 publications

Toll ligand Spätzle3 controls melanization in the stripe pattern formation in caterpillars

Toll ligand Spätzle3 controls melanization in the stripe pattern formation in caterpillars

Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity

The effects of ER morphology on synaptic structure and function in Drosophila melanogaster

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