Sexual dimorphism in the Drosophila hematopoietic organ - the lymph gland

Abstract

Sexual dimorphism is seen at various levels of organization, from gene expression to cellular physiology to animal behavior. Humans show sexual dimorphism in body size, organ size and physiology, and immune responses. Studies in mice have shown that sexual dimorphisms in hematopoietic dynamics can result in sexually dimorphic immune activity that resembles human immune physiology. However, mechanisms underlying these sexual dimorphisms remain poorly understood owing to the complexity of mammalian hematopoiesis. Here, we use the hematopoietic organ of Drosophila melanogaster, the lymph gland, to characterize sexual dimorphism in hematopoiesis and understand the signaling pathways underlying it. The highly conserved signaling pathways in the lymph gland, the relatively simple blood cell lineage, and the vast transgenic tools make flies an ideal system for exploring sexual dimorphism in hematopoiesis. In this thesis project, we find that female lymph glands are bigger and house more mature blood cells than males showing that D. melanogaster exhibits sexual dimorphism in lymph gland morphology. We also show that only the female lymph glands express robust levels of the sex determination pathway gene sex-lethal showing that the fly sex determination pathway is active in the lymph glands. We also identify a previously unknown role of the sex determination pathway gene transformer in the larval fat body and brain in non-cell autonomously regulating lymph gland size and crystal cell differentiation. Finally, we show that the lymph glands respond to chronic E. coli infection in a sexually dimorphic manner. Together, our study identifies underlying mechanisms for the emergence of sexual dimorphism in fly hematopoiesis that can help understand the cause and effect of sexual dimorphism observed in mammalian hematopoiesis. In the future, this can help develop sex-specific therapies for cancers, metabolic disorder-associated inflammation, and pathogenic infections.