The <i>Drosophila</i> Atypical Protein Kinase C-Ref(2)P Complex Constitutes a Conserved Module for Signaling in the Toll Pathway

Avila, A.; Silverman, Neal S.; Diaz-Meco, Marı́a T.; Moscat, Jorge

doi:10.1128/mcb.22.24.8787-8795.2002

Cited by 62 publications

(56 citation statements)

References 43 publications

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“…In this regard, PKCz is capable of phosphorylating directly Dif, which suggests a high degree of conservation of PKCz in the NF-kB pathways. 30 Notably, recent data confirmed these observations by direct injection of doublestranded RNA of Drosophila PKCz and Ref (2)P into Drosophila adult flies. 31 …”

Section: The Atypical Pkcf In the Drosophila Immune Responsesupporting

confidence: 72%

“…56 Interestingly, p62 was shown to be required for NF-kB signaling in several systems [57][58][59] including Drosophila, in which a functionally relevant homolog termed Ref(2)P was identified. 30 This protein has an overall structure very similar to that of p62 (Figure 4), suggesting that it may be a critical mediator of NF-kB in Drosophila cells in partnership with PKCz. In fact, the knockdown of Ref(2)P with RNAi in Drosophila cells leads to the impairment of Drosomycin expression.…”

Section: Adapters and The Specificity During Cell Signalingmentioning

confidence: 94%

“…Interestingly, knocking down PKCz with RNAi in Drosophila cells dramatically inhibits drosomycin expression but not that of diptericin, indicating that PKCz is located specifically in the Toll antifungal pathway. 30 Remarkably, PKCz downmodulation does not affect Cactus or Relish degradation, but it does inhibit the drosomycin promoter activity of a luciferase reporter plasmid. Therefore, in Drosophila, like in mammalian cells, PKCz is necessary for NF-kB transcriptional activity, but not for the control of the nuclear translocation of RelA or Dorsal/Dif.…”

Section: The Atypical Pkcf In the Drosophila Immune Responsementioning

confidence: 99%

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PKCζ at the crossroad of NF-κB and Jak1/Stat6 signaling pathways

2005

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The atypical protein kinase C (PKC) isoforms (aPKC) have been implicated in the regulation of a number of essential signaling events. Early studies using dominant-negative mutants suggested that they are important intermediaries in the activation of the canonical nuclear factor (NF)-jB pathway. More recent data using knockout mice genetically demonstrate that in fact the PKCf isoform is essential for the adequate activation of this cascade both upstream and downstream the IjB kinase complex. In this review, we summarize the mechanistic details whereby the aPKC pathway regulates important cellular functions and how this is achieved by the ability of these kinases to interact with different protein regulators and adapters, as well as to impinge in NF-jB-independent signaling cascades such as the Janus kinase-1/signal transducer and activator of transcription 6 system, which plays a critical role in T-cellmediated hepatitis and asthma.

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Section: The Atypical Pkcf In the Drosophila Immune Responsesupporting

confidence: 72%

Section: Adapters and The Specificity During Cell Signalingmentioning

confidence: 94%

Section: The Atypical Pkcf In the Drosophila Immune Responsementioning

confidence: 99%

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PKCζ at the crossroad of NF-κB and Jak1/Stat6 signaling pathways

2005

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“…The reasons for this are unclear, but it may simply be that there is only a very small viral titer in zygotes, so that genes that reduce viral replication can entirely cure flies of the infection at this stage. Previous studies have suggested that ref(2)P encodes a protein that functions in the Toll pathway (Avila et al 2002), which is an important immune pathway in D. melanogaster, although any possible anti-viral functions are still not clear.…”

Section: Maternal Transmission To Homozygous Offspringmentioning

confidence: 99%

“…ref(2)P encodes a protein that is thought to function both in sperm development and in the Toll pathway (an important component of the innate immune system) (Dezelee et al 1989;Avila et al 2002). A complex mutation in ref(2)P reduces the replication rate of the sigma virus (Brun and Plus 1980;Carre-Mlouka et al 2007).…”

Section: G Enetic Variation Affects Disease Resistance In Amentioning

confidence: 99%

Genetic Variation Affecting Host–Parasite Interactions: Different Genes Affect Different Aspects of Sigma Virus Replication and Transmission in Drosophila melanogaster

et al. 2008

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In natural populations, genetic variation affects resistance to disease. Knowing how much variation exists, and understanding the genetic architecture of this variation, is important for medicine, for agriculture, and for understanding evolutionary processes. To investigate the extent and nature of genetic variation affecting resistance to pathogens, we are studying a tractable model system: Drosophila melanogaster and its natural pathogen the vertically transmitted sigma virus. We show that considerable genetic variation affects transmission of the virus from parent to offspring. However, maternal and paternal transmission of the virus is affected by different genes. Maternal transmission is a simple Mendelian trait: most of the genetic variation is explained by a polymorphism in ref (2)P, a gene already well known to affect resistance to sigma. In contrast, there is considerable genetic variation in paternal transmission that cannot be explained by ref (2)P and is caused by other loci on chromosome 2. Furthermore, we found no genetic correlation between paternal transmission of the virus and resistance to infection by the sigma virus following injection. This suggests that different loci affect viral replication and paternal transmission.

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Interleukin-1 Receptor/Toll-Like Receptor Signaling

Wajant

Scheurich

Henkler

Toll and Toll-Like Receptors: An Immunologic Perspective

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The Drosophila Atypical Protein Kinase C-Ref(2)P Complex Constitutes a Conserved Module for Signaling in the Toll Pathway

Cited by 62 publications

References 43 publications

PKCζ at the crossroad of NF-κB and Jak1/Stat6 signaling pathways

PKCζ at the crossroad of NF-κB and Jak1/Stat6 signaling pathways

Genetic Variation Affecting Host–Parasite Interactions: Different Genes Affect Different Aspects of Sigma Virus Replication and Transmission in Drosophila melanogaster

Interleukin-1 Receptor/Toll-Like Receptor Signaling

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