The Participation of Prophenoloxidase in the Drosophila Anti-nematode Innate Immune Response
Open AccessDrosophila melanogaster relies on an evolutionarily conserved innate immune system to protect itself from potentially deadly pathogens. One of the earliest pathways activated after injury or infection is the melanization pathway, which is responsible for synthesizing and depositing melanin at the site of injury, or onto invading microbes. Three genes, PPO1-3, encoding prophenoloxidase (PPO) are responsible for the production of melanin after their activation to phenoloxidase (PO) when injury or infection is detected. One pathogen capable of infecting D. melanogaster are entomopathogenic nematodes. Steinernema carpocapsae nematodes exist in a mutualistic relationship with Xenorhabdus nematophila bacteria and are an important biological control agent for controlling insect pests. The nematode-bacteria complex (symbiotic nematodes) can be separated, creating “axenic” nematodes, devoid of bacteria, which are still capable of infecting and killing D. melanogaster. In order to investigate how the D. melanogaster melanization pathway contributes to the anti-nematode immune response, symbiotic and axenic S. carpocapsae were used to study D. melanogaster survival, PPO gene expression, and activation of PPO to PO. Research shows that expression of all three D. melanogaster PPO genes contribute to survival, however none appear to be up- regulated during nematode infection. Further, we found that axenic nematode infection leads to higher levels of PO, suggesting that X. nematophila suppresses this activation.We also report for the first time the differentiation of lamellocytes, a specialized type of hemocyte in D. melanogaster, in response to symbiotic S. carpocapsae nematode infection. Our results suggest an important role played by the melanization pathway in response to nematode infection, and demonstrate how this response can be manipulated by S. carpocapsae nematodes and their mutualistic X. nematophila bacteria.
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