Tribolium castaneum gene expression changes after Paranosema whitei infection

Alberto Lopez-Ezquerra; Andreas Mitschke; Erich Bornberg-Bauer; Gerrit Joop

doi:10.1016/j.jip.2018.02.009

Tribolium castaneum gene expression changes after Paranosema whitei infection

J Invertebr Pathol. 2018 Mar:153:92-98. doi: 10.1016/j.jip.2018.02.009. Epub 2018 Feb 13.

Authors

Alberto Lopez-Ezquerra¹, Andreas Mitschke², Erich Bornberg-Bauer³, Gerrit Joop²

Affiliations

¹ Molecular Evolution and Bioinformatics, Institute for Evolution and Biodiversity, Germany. Electronic address: a.lopez@uni-muenster.de.
² Justus-Liebig-Universität Giessen, Germany.
³ Molecular Evolution and Bioinformatics, Institute for Evolution and Biodiversity, Germany.

PMID: 29452083
DOI: 10.1016/j.jip.2018.02.009

Abstract

Background: Microsporidia are obligate parasites that possess some of the smallest eukaryotic genomes. Several insect species are susceptible to infections by microsporidian parasites. Paranosema whitei frequently infects young larvae of Tribolium castaneum and obligately kills the host whereupon transmission to subsequent hosts is accomplished via spores. P. whitei infection results in developmental arrest of T. castaneum, preventing larvae from pupation. The mechanisms underlying P. whitei virulence as well as the molecular underpinning of host defenses remain uncharacterized. In the present study, we evaluated gene expression differences of T. castaneum infected with the microsporidian parasite P. whitei.

Results: More than 1500 T. castaneum genes were differentially expressed after infection with P. whitei. Several important host pathways appeared to be differentially expressed after infection, where immune genes were among the highest differential expressed genes. Genes involved in the Toll pathway and its effectors were specifically upregulated. Furthermore, iron homeostasis processes and transmembrane transport appeared significantly altered after P. whitei infection. Krüppel homolog 1 (Kr-h1) and other genes of the juvenile hormone (JH) pathway appeared differentially expressed after parasite infection. In addition, a small number of long intergenic non-coding RNAs (lincRNAs) appeared differentially expressed after P. whitei infection.

Conclusion: In this study we characterized for the first time using RNA-seq the immune response of T. castaneum to P. whitei. Other pathways (transmembrane transport, iron homeostasis, protein synthesis, JH) indicate possible alterations of the host by the parasite such as a possible developmental arrest caused by JH regulation. Furthermore we find evidence that some lincRNAs might be connected to defense as previously reported for other insect species.

Keywords: Host-parasite interactions; JH; LincRNA; Microsporidia; Transcriptomics.

MeSH terms

Animals
Gene Expression Regulation / physiology*
Host-Parasite Interactions / genetics*
Juvenile Hormones / genetics
Nosema*
Tribolium / immunology
Tribolium / parasitology*

Substances

Juvenile Hormones