PHYSIOLOGICAL GENETICS OF MELANOTIC TUMORS IN DROSOPHILA MELANOGASTER. II. THE GENETIC BASIS OF RESPONSE TO TUMORIGENIC TREATMENTS IN THE <i>tu K</i> AND <i>tu bw; st su-tu</i> STRAINS

Burnet, Barrie; Sang, James H.

doi:10.1093/genetics/49.2.223

Cited by 14 publications

(2 citation statements)

References 8 publications

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“…Here, we focus on Drosophila mutants that mount misdirected immune responses against their own tissues. Surprisingly, numerous classical Drosophila mutant strains known as melanotic tumor mutants, in which blood cells attack and encapsulate aberrant self tissues due to a deficiency in self-tolerance, were never fully genetically characterized ( 35 – 40 ). Of those still available in public stock collections ( SI Appendix , Table S1 ), we decided to characterize the D. melanogaster tumor(1)Suzuki ( tuSz ) melanotic tumor strain, which was isolated in a large-scale temperature-sensitive mutagenesis screen ( 41 , 42 ).…”

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confidence: 99%

Extracellular matrix protein N-glycosylation mediates immune self-tolerance inDrosophila melanogaster

Mortimer

Fischer

Waring

et al. 2021

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

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In order to respond to infection, hosts must distinguish pathogens from their own tissues. This allows for the precise targeting of immune responses against pathogens and also ensures self-tolerance, the ability of the host to protect self tissues from immune damage. One way to maintain self-tolerance is to evolve a self signal and suppress any immune response directed at tissues that carry this signal. Here, we characterize the Drosophila tuSz1 mutant strain, which mounts an aberrant immune response against its own fat body. We demonstrate that this autoimmunity is the result of two mutations: 1) a mutation in the GCS1 gene that disrupts N-glycosylation of extracellular matrix proteins covering the fat body, and 2) a mutation in the Drosophila Janus Kinase ortholog that causes precocious activation of hemocytes. Our data indicate that N-glycans attached to extracellular matrix proteins serve as a self signal and that activated hemocytes attack tissues lacking this signal. The simplicity of this invertebrate self-recognition system and the ubiquity of its constituent parts suggests it may have functional homologs across animals.

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mentioning

confidence: 99%

Extracellular matrix protein N-glycosylation mediates immune self-tolerance inDrosophila melanogaster

Mortimer

Fischer

Waring

et al. 2021

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

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“…F-TRP plasma concentrations are affected by the levels of its carrier, albumin (ALB), and free fatty acids (FFA) competing with TRP for ALB binding sites. The lack of correlation between F-TRP, ALB and FFA in cancer patients has shown a tumor-dependent effect on the rise in F-TRP [10][11].…”

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confidence: 99%

Tumor Induction Studies in Drosophila Melanogaster Using Tryptophan

V¹,

PRIYANKA²

2011

Int J Med Clin Res

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Tumor cells have an altered amino acid metabolism. They express high levels of tryptophan and L-arginine metabolizing enzymes. This leads to depletion of tryptophan and L-arginine and locally blocks T cell proliferation. Therefore, the characteristic energy metabolism of tumor cells leads to immune suppression and contributes to immune escape processes at the tumor site [1]. Excess dietary Tryptophan has shown to cause increased tumor incidence in tumorous strains of Drosophila [2]. Canton (wild type) flies were exposed to 10mM, 20mM, 30mM, 40mM and 50mM concentrations of Tryptophan. Phenotypic analysis of the exposed flies and qualitative analysis of the isolated DNA was done 24 hours and 48 hours after exposure to Tryptophan. The quality of the DNA was evaluated using Nanodrop and the DNA was subjected to Fragmentation assay to study the damage induced. Phenotypic changes observed were elongated abdomen with distinct curling and discoloration of thorax to mild orange. The isolated DNA was found to be of good quality and the fragmentation assay showed patterns of shearing. As the damage observed was not significant and the tumor induction was not observed in the experimental concentrations, tryptophan was considered non tumorigenic at the above said concentrations. However, higher concentrations of Tryptophan may induce tumor.

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An amino acid substitution in the Drosophila hopTum-l Jak kinase causes leukemia-like hematopoietic defects.

1995

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Proteins of the Jak family of non‐receptor kinases play important roles in mammalian hematopoietic signal transduction. They mediate the cellular response to a wide range of cytokines and growth factors. A dominant mutation in a Drosophila Jak kinase, hopscotchTumorous‐lethal (hopTum‐l), causes hematopoietic defects. Here we conduct a molecular analysis of hopTum‐l. We demonstrate that the hopTum‐l hematopoietic phenotype is caused by a single amino acid substitution of glycine to glutamic acid at residue 341. We generate a true revertant of the hopTum‐l mutation, in which both the molecular lesion and the mutant hematopoietic phenotype revert back to wild type. We also examine the effects of the G341E substitution in transgenic flies. The results indicate that a mutant Jak kinase can cause leukemia‐like abnormalities.

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PHYSIOLOGICAL GENETICS OF MELANOTIC TUMORS IN DROSOPHILA MELANOGASTER. II. THE GENETIC BASIS OF RESPONSE TO TUMORIGENIC TREATMENTS IN THE tu K AND tu bw; st su-tu STRAINS

Cited by 14 publications

References 8 publications

Extracellular matrix protein N-glycosylation mediates immune self-tolerance inDrosophila melanogaster

Extracellular matrix protein N-glycosylation mediates immune self-tolerance inDrosophila melanogaster

Tumor Induction Studies in Drosophila Melanogaster Using Tryptophan

An amino acid substitution in the Drosophila hopTum-l Jak kinase causes leukemia-like hematopoietic defects.

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