PreprintArticleVersion 1This version is not peer-reviewed
Macrophage-Like Blood Cells Are Involved in Inter-Tissue Communication to Activate JAK/STAT Signaling That Induces Antitumor Turandot Proteins in Drosophila Fat Body via the TNF-JNK Pathway
Version 1
: Received: 7 October 2024 / Approved: 9 October 2024 / Online: 10 October 2024 (02:40:27 CEST)
How to cite:
Kinoshita, J.; Kinoshita, Y.; Nomura, T.; Inoue, A. Y. H. Macrophage-Like Blood Cells Are Involved in Inter-Tissue Communication to Activate JAK/STAT Signaling That Induces Antitumor Turandot Proteins in Drosophila Fat Body via the TNF-JNK Pathway. Preprints2024, 2024100708. https://doi.org/10.20944/preprints202410.0708.v1
Kinoshita, J.; Kinoshita, Y.; Nomura, T.; Inoue, A. Y. H. Macrophage-Like Blood Cells Are Involved in Inter-Tissue Communication to Activate JAK/STAT Signaling That Induces Antitumor Turandot Proteins in Drosophila Fat Body via the TNF-JNK Pathway. Preprints 2024, 2024100708. https://doi.org/10.20944/preprints202410.0708.v1
Kinoshita, J.; Kinoshita, Y.; Nomura, T.; Inoue, A. Y. H. Macrophage-Like Blood Cells Are Involved in Inter-Tissue Communication to Activate JAK/STAT Signaling That Induces Antitumor Turandot Proteins in Drosophila Fat Body via the TNF-JNK Pathway. Preprints2024, 2024100708. https://doi.org/10.20944/preprints202410.0708.v1
APA Style
Kinoshita, J., Kinoshita, Y., Nomura, T., & Inoue, A. Y. H. (2024). Macrophage-Like Blood Cells Are Involved in Inter-Tissue Communication to Activate JAK/STAT Signaling That Induces Antitumor Turandot Proteins in Drosophila Fat Body via the TNF-JNK Pathway. Preprints. https://doi.org/10.20944/preprints202410.0708.v1
Chicago/Turabian Style
Kinoshita, J., Tadashi Nomura and and Yoshihiro H. Inoue. 2024 "Macrophage-Like Blood Cells Are Involved in Inter-Tissue Communication to Activate JAK/STAT Signaling That Induces Antitumor Turandot Proteins in Drosophila Fat Body via the TNF-JNK Pathway" Preprints. https://doi.org/10.20944/preprints202410.0708.v1
Abstract
Turandot (Tot) family proteins, which are induced via the JAK/STAT pathway after infection, also suppress lymph gland tumors in Drosophila mxcmbn1 mutant larvae. We investigated the potential role of hemocytes in Tot induction in tumor-bearing mutants by immunostaining and RNAi experiments. Normal hemocytes transplanted into mutant larvae were recruited to the tumor and fat body (FB), suggesting that these cells transmit tumor-related information. The transplanted hemocytes ectopically expressed Unpaired3 (Upd3), which is necessary to activate JAK/STAT. Eiger, a Drosophila Tumor necrosis factor (TNF) ortholog, was highly expressed in tumors. Depletion of the Eiger receptor in hemocytes reduced Tot levels and eventually enhanced tumor growth. The c-Jun N-terminal kinase (JNK) pathway, acting downstream of the receptor, was also activated in the hemocytes of mutants. Downregulation of the JNK pathway in hemocytes inhibited Tot induction, leading to enhanced tumor growth. These results suggest that the upd3 expression in hemocytes depends on the Eiger-JNK pathway. We propose that after Eiger activates the JNK pathway in hemocytes on the tumor, cells expressing Upd3 are recruited to the FB. Upd3 then activates JAK/STAT to induce the expression of antitumor proteins. This study highlights the intricate communication between tissues via blood cells during tumor suppression.
Biology and Life Sciences, Cell and Developmental Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
