Macrophage-derived upd3 cytokine causes impaired glucose homeostasis and reduced lifespan in Drosophila fed a lipid-rich diet.

Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic activation of JAK-STAT signaling, reduced insulin sensitivity, hyperglycemia, and a shorter lifespan. Drosophila macrophages produced the JAK-STAT-activating cytokine upd3, in a scavenger-receptor (crq) and JNK-dependent manner. Genetic depletion of macrophages or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-κB signaling made no contribution to the phenotype observed. These results identify an evolutionarily conserved "scavenger receptor-JNK-type 1 cytokine" cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway.

The genome sequence of the hoverfly, Epistrophella euchroma (Kowarz, 1885).

We present a genome assembly from an individual male Epistrophella euchroma (hoverfly, Arthropoda; Insecta; Diptera; Syrphidae). The genome sequence is 523.3 megabases in span. Most of the assembly is scaffolded into 6 chromosomal pseudomolecules, including the X and Y sex chromosomes. The mitochondrial genome has also been assembled and is 17.24 kilobases in length.

The genome sequence of the bulrush Neoascia, Neoascia interrupta (Meigen, 1822).

We present a genome assembly from an individual female Neoascia interrupta (the bulrush Neoascia; Arthropoda; Insecta; Diptera; Syrphidae). The genome sequence is 601.9 megabases in span. Most of the assembly is scaffolded into 4 chromosomal pseudomolecules, including the X sex chromosome. The mitochondrial genome has also been assembled and is 17.76 kilobases in length. Gene annotation of this assembly on Ensembl identified 22,086 protein coding genes.

The genome sequence of the white-footed hoverfly, Platycheirus albimanus (Fabricius, 1781).

We present a genome assembly from an individual female Platycheirus albimanus (the white-footed hoverfly; Arthropoda; Insecta; Diptera; Syrphidae). The genome sequence is 677.8 megabases in span. Most of the assembly is scaffolded into 4 chromosomal pseudomolecules, including the X sex chromosome. The mitochondrial genome has also been assembled and is 18.17 kilobases in length. Gene annotation of this assembly on Ensembl identified 12,568 protein coding genes.

Adult Drosophila Lack Hematopoiesis but Rely on a Blood Cell Reservoir at the Respiratory Epithelia to Relay Infection Signals to Surrounding Tissues.

The use of adult Drosophila melanogaster as a model for hematopoiesis or organismal immunity has been debated. Addressing this question, we identify an extensive reservoir of blood cells (hemocytes) at the respiratory epithelia (tracheal air sacs) of the thorax and head. Lineage tracing and functional analyses demonstrate that the majority of adult hemocytes are phagocytic macrophages (plasmatocytes) from the embryonic lineage that parallels vertebrate tissue macrophages. Surprisingly, we find no sign of adult hemocyte expansion. Instead, hemocytes play a role in relaying an innate immune response to the blood cell reservoir: through Imd signaling and the Jak/Stat pathway ligand Upd3, hemocytes act as sentinels of bacterial infection, inducing expression of the antimicrobial peptide Drosocin in respiratory epithelia and colocalizing fat body domains. Drosocin expression in turn promotes animal survival after infection. Our work identifies a multi-signal relay of organismal humoral immunity, establishing adult Drosophila as model for inter-organ immunity.

Multiple TGF-ß superfamily signals modulate the adult Drosophila immune response.

TGF-ß superfamily signals play complex roles in regulation of tissue repair and inflammation in mammals [1]. Drosophila melanogaster is a well-established model for the study of innate immune function [2, 3] and wound healing [4-7]. Here, we explore the role and regulation of two TGF-ß superfamily members, dawdle and decapentaplegic (dpp), in response to wounding and infection in adult Drosophila. We find that both TGF-ß signals exhibit complex regulation in response to wounding and infection, each is expressed in a subset of phagocytes, and each inhibits a specific arm of the immune response. dpp is rapidly activated by wounds and represses the production of antimicrobial peptides; flies lacking dpp function display persistent, strong antimicrobial peptide expression after even a small wound. dawdle, in contrast, is activated by Gram-positive bacterial infection but repressed by Gram-negative infection or wounding; its role is to limit infection-induced melanization. Flies lacking dawdle function exhibit melanization even when uninfected. Together, these data imply a model in which the bone morphogenetic protein (BMP) dpp is an important inhibitor of inflammation following sterile injury whereas the activin-like dawdle determines the nature of the induced immune response.