Differential gene expression linked to parasitic and mycetophagous forms of Deladenus siricidicola in culture

Abstract

The nematode, Deladenus siricidicola is an important biological control agent of the Sirex noctilio woodwasp. Deladenus siricidicola alternates between a mycetophagous/free-living and parasitic life cycle. The free-living life cycle can be maintained indefinitely on its food source, the fungus Amylostereum areolatum. In the parasitic life cycle a pronounced stylet is present in the adult females, differentiating it from the free-living nematodes. In the parasitic life cycle the nematode infects the S. noctilio larvae and subsequently sterilises the eggs in the developing adult. Little is known about the molecular mechanisms underlying these life stages. The aim of this study was to investigate the expression of genes potentially associated with the free-living and the parasitic life cycle of D. siricidicola. The development of the parasitic life cycle was successfully stimulated in vitro through the use of lactic acid by lowering the pH of the culture media. Significantly up- and down-regulated genes were identified from RNA sequencing data from both free-living and parasitic life cycle samples. Genes putatively involved in the host immune modulation and nematode survival inside the host using homology-based methods were also identified. Genes of interest included enzymes such as glycoside hydrolase, cysteine proteinase and phosphatidylinositol-3-kinase. Glycoside hydrolase is important for chitin degradation which is found in fungal cell walls and insect cuticles. The cysteine proteinase and phosphatidylinositol-3-kinase seem to be important in egg yolk degradation, host entry and conversion ability of the nematode. This study lays the foundation for future studies on the molecular regulation of the bicyclic D. siricidicola life stages and its interaction with its host S. noctilio, and opens the door for attempts to select strains of this nematode for a more effective biological control programme.