Transcriptome analysis of Nosema assamensis infecting muga silkworms (Antheraea assamensis) reveals insights into candidate pathogenicity related genes and molecular pathways required for pathogenesis.

Abstract

Muga silkworms are often prone to many diseases since, these are non-domesticated and are reared outdoors. Microsporidia, an obligate intracellular pathogen with spore as its active form, causes pebrine disease in these silkworms. The study has attempted to categorise the transcript data of the Nosema obtained from the infected muga silkworm using gene ontology and KEGG pathway studies. A total of 2850 unigene sets were identified out of which 2739 unigenes were placed under biological, cellular as well as molecular function categories based on the gene ontology (GO) terms. 1620 out of these unigenes sets found their orthologous partner in the corresponding Nosema bombycis transcriptome. The unigenes were found to be enriched under organic substance metabolic process, organic cyclic compound binding and intracellular anatomical structure for biological process, molecular function and cellular components respectively. The KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis indicated majority of the enzymes were found to be mapped under purine and thiamine metabolic pathways, indicating an increase in the energy metabolism required to establish the infection in the silkworms. The putative virulence genes identified in this study are PTP2, PTP3, SWP12 and SWP26 which were found to be expressed in other Nosema species indigenous to India, indicating a probable conservation of these genes, which are primarily involved in establishing host pathogen interactions. The expression of these genes was in detectable levels in the infected silkworm samples. These genes may be validated further through bioassay in order understand their roles in establishing the infection and propagation of the spores. The identified virulence genes may be further targeted to develop diagnostic tools for identification of the pathogen at early stages of infection.