Lopez-Ezquerra, A. Mitschke, A. Bornberg-Bauer, E. and Joop G.
Tribolium castaneum gene expression changes after Paranosema whitei infection
, 2017

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Abstract

Background:
Microsporidia are obligate parasites that possess one of the small-
est eukaryotic genomes. Several insect species are susceptible to infections by mi-
crosporidia parasites. Paranosema whitei frequently infects young larvae of Tribolium
castaneum and obligately kills the host whereupon transmission to subsequent hosts
is accomplished by spores. P. whitei infection results in developmental arrest of T.
castaneum, preventing larvae from pupation. P. whitei virulence mechanisms re-
main to this date uncharacterized, similarly as molecular mechanisms used by the
host for defense. In the present study, we evaluated gene expression differences of T.
castaneum infected with the microsporidian parasite P. whitei.

Results:

More than 1,500 T. castaneum genes were differentially expressed after
infection with P. whitei. Several important host pathways appeared to be altered
after infection, where immune genes were among the highest differential expressed
genes. Genes involved in the Toll pathway and its effectors were specifically up-
regulated. 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 ex-
pressed after parasite infection. In addition, a small number of 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.