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A polydnavirus-encoded ANK protein has a negative impact on steroidogenesis and development
Marilena Ignesti1, Rosalba Ferrara2, Patrizia Romani3
1Dipartimento di Farmacia e Biotecnologie, Università di Bologna, Via Selmi 3 Bologna, Italy.
Insect Biochemistry and Molecular Biology
|March 22, 2018
Summary
Polydnaviruses disrupt moth development. This study shows viral ankyrin TnBVANK3 blocks insect growth by impairing ecdysone production and altering insulin signaling in prothoracic glands.
Area of Science:
- Virology
- Insect Molecular Biology
- Developmental Biology
Background:
- Polydnaviruses (PDV) are essential symbionts of parasitic wasps, impacting host development and immunity.
- While PDV's immunosuppressive roles are known, PDV factors affecting host development remain understudied.
- Ankyrin genes encoded by PDV are implicated in disrupting host physiology.
Purpose of the Study:
- To investigate the role of the polydnavirus ankyrin gene TnBVANK3 in disrupting host development.
- To elucidate the mechanism by which TnBVANK3 affects insect development, specifically ecdysone biosynthesis.
- To understand the interaction between TnBVANK3 and host signaling pathways like insulin/TOR.
Main Methods:
- Utilizing Drosophila melanogaster as a model system to study the function of viral ankyrin genes.
- Expressing TnBVANK3 in Drosophila prothoracic gland (PG) cells to observe its effects on development.
- Analyzing gene expression related to steroidogenesis and insulin/TOR signaling pathways.
- Assessing the impact of insulin pathway activation on pupariation defects.
Main Results:
- TnBVANK3 expression in Drosophila PG blocks the larval-pupal transition.
- TnBVANK3 impairs ecdysone biosynthesis by downregulating steroidogenic genes.
- TnBVANK3 affects genes in the insulin/TOR signaling pathway.
- Constitutive activation of the insulin pathway in PG rescues TnBVANK3-induced pupariation defects.
Conclusions:
- TnBVANK3 acts as a potent virulence factor disrupting insect development.
- TnBVANK3 disrupts ecdysone biosynthesis through a novel mechanism distinct from TnBVANK1.
- TnBVANK3 and TnBVANK1 exhibit synergistic yet non-overlapping functions in disrupting host development.
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