Project description:Parasites can facilitate their own spread and reproduction by manipulating insect hosts behavior, as seen in the interaction between Thitarodes xiaojinensis and Ophiocordyceps sinensis. Infection by O. sinensis leads to the mummification of T. xiaojinensis larvae, but the underlying mechanisms remain mysterious. To uncover this parasitic relationship, metabolites were analyzed in infected and mummified larvae of T. xiaojinensis in this study. Significant changes were found in phenotype, fungal morphology in hemocoel, larval hardness, and mannitol metabolites in infected, mummified 0 h larvae and larvae 5 days after mummification behavior. Surprisingly, the occurrence of mummification behavior was accompanied by fungal dimorphism, as well as the absence of mannitol in both infected and non-infected larvae, until the initial accumulation of mannitol and the expression of mannitol-associated genes occurred at the time of mummification behavior. The presence of mannitol may promote fungal dimorphism to mediate changes in fungal toxicity or resistance, leading to the end of the fungus-insect coexistence period and the incidence of mummification behavior. Furthermore, mannitol injections increase the mummification rate of the infected larvae without significant difference from the normal mummification phenotype. This finding suggests the importance of mannitol in the mummification of host larvae infected with O. sinensis.
Project description:<p>Parasites can manipulate host behavior to facilitate parasite transmission. One such host-pathogen interaction occurs between the fungus Ophiocordyceps sinensis (O. sinensis) and the ghost moth Thitarodes xiaojinensis. O. sinensis is involved in the mummification process of infected host larvae. However, the underlying molecular and chemical mechanism for this phenomenon is unknown. We characterized the small molecules regulating host behavior and the altered metabolites in infected and mummified host larvae. Lipid-related metabolites, such as phosphatidylcholine (PC) were identified in infected and mummified larvae. Decreased levels of the neurotransmitter acetylcholine (ACh) and elevated choline levels were observed in the brains of both the infected and mummified larvae. The aberrant activity of acetylcholinesterase (AChE) and relative mRNA expression of ACE2 (acetylcholinesterase) may mediate the altered transformation between ACh and choline, leading to the brain dysfunction of mummified larvae. Caspofungin treatment inhibited the mummification of infected larvae and the activity of AChE. These findings indicate the importance of ACh in the mummification of host larvae after O. sinensis infection.</p><p><br></p><p><strong>Metabolome data</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS9929' rel='noopener noreferrer' target='_blank'><strong>MTBLS9929</strong></a>.</p><p><strong>Lipidome data</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS9930' rel='noopener noreferrer' target='_blank'><strong>MTBLS9930</strong></a>.</p>