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The role of Akh in the systemic gene expression changes induced by Drosophila C Virus infection

ABSTRACT: Drosophila C Virus (DCV) is a natural pathogen that induces profound systemic wasting and metabolic dysfunction in Drosophila melanogaster. In this study, we identify Adipokinetic Hormone (Akh), a functional analog of mammalian glucagon, as a central endocrine mediator of this process. Our results show that DCV infection robustly increases Akh production and signaling, which correlates closely with the progression of host wasting phenotypes, including lipid loss, hyperglycemia, muscle dysfunction, and ovary atrophy. To elucidate the transcriptomic basis of Akh-mediated wasting, we performed RNA-sequencing (RNA-seq) on whole-body samples from four groups: wild-type (WT) and Akh-null mutant flies, each challenged with either PBS (control) or DCV. Differential expression analysis reveals that a significant subset of genes (183 up-regulated and 308 down-regulated) are modulated by DCV in an Akh-dependent manner. These genes are primarily enriched in pathways associated with carbohydrate, lipid, and protein metabolism. Notably, while DCV infection also affects the systemic insulin pathway and various stress-related signaling axes (e.g., Jak/Stat, TNF/JNK), these alterations occur largely independently of Akh. Our findings suggest that Akh drives infection-induced energy wasting through a distinct regulatory axis. This dataset provides a comprehensive resource for understanding the endocrine mechanisms governing host-pathogen interactions and metabolic homeostasis.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE326139 | GEO | 2026/03/28

REPOSITORIES: GEO

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