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Decision letter

We then assessed the resulting fish for green fluorescence and compared them with those injected with the HuC:Gal4 construct alone. At 48 hpf, the Gal80 expressing animals did not show any fluorescence, whereas control actin gal4 expressed Kaede in scattered neurons Fig.

The Gal80 Actin gal4 embryos begun to express Kaede at 3 dpf, whose fluorescence peaked at 7 dpf, albeit less intensely than in control animals Fig. These observations demonstrate that Gal80 is an efficient repressor of Gal4 in neural tissues. actin gal4


They also actin gal4 that the gradual release of Gal4 inhibition likely due to the degradation of the Gal80 allows the expression of the UAS-driven genes at later stages of development with an average onset at 4 dpf. In H, asterisks indicate the fish displaying Actin gal4. Representative specimens are depicted at 48 hpf, 3 and 7 dpf. We tested whether Gal4 repression by Gal80 was dose-dependent. We co-injected eggs from this line with a cDNA coding for the full-length Gal4 under the transcriptional control of the beta-actin promoter for ubiquitous expression, together with different concentrations of Gal80 synthetic mRNA Fig. Starting at 4 dpf, all fish groups were strongly fluorescent but the pg group continued to exhibit lower fluorescence Fig.

FlyBase Recombinant Construct Report: P{Act5C-GAL4}

In order to quantify the actin gal4 activity of Gal80, we looked at the level of Td-Tomato expression at different time actin gal4 in cells from fish injected with increasing concentrations of Gal80 RNA Fig. For each condition, we selected individual cells and imaged them at 3, 4 and 6 dpf Fig.

  • FlyBase Recombinant Construct Report: P{Act5C-GAL4}
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  • GAL4/UAS system

The reviewers have discussed the reviews with one another and the Reviewing Editor has drafted this decision to help you prepare a revised submission. Previous studies in the mammalian system have shown that F-actin is a ligand released from necrotic cells that binds to and activates DNGR1 in dendritic cells to promote cross presentation of dead cell-associated antigens. Expanding on these studies, Srinivasan et al. Indeed, they found that injection of actin into Drosophila triggered induction of STAT-dependent genes. Analogous to the actin-DNGR1 pathway in mammals, the actin signaling pathway in Drosophila requires non-receptor tyrosine kinases Shark and Src42A, which are Drosophila orthologues of the mammalian kinases Syk and Src, respectively. The actin sensing and signaling pathway appears to operate also in fat body cells, which are proposed to produce Upd3 that then functions in an autocrine or paracrine manner to activate the Domeless-JAK-STAT pathway in the fat body.

The role of the actin-sensing pathway in infection or sterile inflammation also remains to be determined in part because it is not practical to perform loss of function studies of actin, which is actin gal4 essential gene; identification of the actin receptor in Drosophila may enable such genetic studies. Nevertheless, this is an important study because it provides convincing evidence for the existence of an innate immune system that detects actin as a DAMP in Drosophila.

This work establishes Drosophila as a model system to study sterile inflammation and suggests that actin is an evolutionarily conserved danger molecule from dead or damaged cells. While the genetic dissection of actin gal4 responses is impressive and compelling, there are conceptual and technical aspects of this work that need to be addressed.

Q-System reagents - flies

While this conclusion is certainly correct, the experiment performed was almost guaranteed to work, as the authors used a STAT-dependent gene in their analysis TotM. It would be highly informative for the authors to also examine actin-inducible genes that are not annotated as STAT-response genes, and genes whose expression is repressed actin gal4 actin injection. Actin gal4 receptors are different DNGR-1 vs. STAT-dependent gene expression in fliesthe responding cell types are different dendritic cells vs fat body in flies and the ligands are different F-actin vs. Despite these differences, the authors suggest an evolutionarily conserved role of actin as a DAMP. Can the authors really say that their evidence supports this evolutionary argument? The authors could back off their argument that this study provides evidence for a conserved need for actin detection, especially in light of their lack of evidence for the importance of actin-dependent responses.

Alternatively, the authors could place this data in the context of other innate immune responses that occur differently in different organisms. Since actin is an ATP binding protein, and the commercial source of the actin used in this study states that the actin solutions contain ATP, this is a legitimate issue. It is formally possible that actin injected into the flies is metabolized, modified or somehow causes tissue injury, which indirectly activates the Src pathway. Thus, some direct evidence, such as that obtained by stimulating fat body cells with actin in a cell culture setting, is necessary to establish actin as a direct ligand.

Ideally, the authors should provide evidence for the importance of actin signaling in a physiological or actin gal4 setting.Also Known As. Act5C-Gal4, actin-GAL4, act-GAL4, Actin5c-GAL4, actGAL4, actin 5C-GAL4, actin-5C-GAL4, Act5CGal4, Gal4-Act5c, actin5CGAL4.


Size. Scer\GAL4. Also Known As. Actin-GAL4, Act-GAL4, actGal4, actinGal4, act5C- GAL4, act>y+>Gal4, actin::Gal4, Act::Gal4, actin>GAL4, Actin Actin gal4. Size.

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