The PI3K/AKT Pathway and PTEN Gene Are Involved in "Tree-Top Disease" of Lymantria dispar.

Fengjiao Li,Christopher Rensing,Long Liu,Xiao Yu,Dun Wang

doi:10.3390/genes13020247

Fengjiao Li, Christopher Rensing + Show 3 more

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https://doi.org/10.3390/genes13020247

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Journal: Genes	Publication Date: Jan 27, 2022
Citations: 1	License type: CC BY 4.0

Affiliation: North West Agriculture and Forestry University

Abstract

Nucleopolyhedrovirus (NPV) can alter its host behaviour such that infected larvae hang at the top of trees before their death. This phenomenon was firstly described by Hofmann in 1891 and named as “tree-top disease”. Subsequent studies have described effects during the infection proceedings as NPVs manipulate the host to avoid the immune response, cross defensive barriers and regulate hormones. In this study, we demonstrate that the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway is involved in host manipulation by Lymantria dispar multiple nucleopolyhedrovirus (LdMNPV). Particularly at the late stage of infection, a multifunctional dephosphorylase in the PI3K/AKT signaling pathway is dynamically upregulated, namely, the phosphatidylinositol-3, 4, 5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase (PTEN) gene. The biological assays of PTEN gene knockdown showed that an increase in PTEN gene expression was necessary for the infected Lymantria dispar larvae’s terminal climbing behavior, death postponement and virion production. The results imply that the PI3K/AKT signaling pathway and PTEN gene might play an essential role in “tree-top disease” induced by LdMNPV.

Highlights

Many parasites manipulate their hosts in various ways via changes to gene expression, cellular metabolism, signal transduction and even behavior to increase fecundity and transmission rates [1,2,3]
As a stable intersection of signal transduction, the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway was activated by different types of growth factors and cellular stimuli regulated by upstream pathways, such as the insulin-like signaling pathway and chemokine signaling pathway
Baculoviruses have been shown to induce a series of behavioral changes in infected larvae including prolonged instars and the behavior of climbing to an elevated location before death [4,5,6]

Summary

Introduction

Many parasites manipulate their hosts in various ways via changes to gene expression, cellular metabolism, signal transduction and even behavior to increase fecundity and transmission rates [1,2,3]. Baculoviruses provide an example of parasite-induced alteration of host behavior and are characterized by a strong behavioral change whereby the infected larvae usually climb to an elevated location before death [4,5,6]. Not all insects alter their behavior by climbing to an elevated location after baculovirus infection [7,8]. Comparing the differentially expressed genes (DEGs) of brains that were infected with BmNPV and healthy silkworms, it was shown that BmNPV-induced hyperactive behavior was correlated with synaptic transmissions, serotonin receptor signaling and circadian rhythm pathways [16]. Intricate and complex fluctuations in the cell program and cellular signaling transduction have been demonstrated

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