Protein tyrosine phosphatases of Toxoneuron nigriceps bracovirus as potential disrupters of host prothoracic gland function

Abstract

The genomic sequence of the bracovirus associated with the wasp Toxoneuron nigriceps (Hymenoptera, Braconidae) (TnBV), an endophagous parasitoid of the tobacco budworm larvae, Heliothis virescens (Lepidoptera, Noctuidae), contains a large gene family coding for protein tyrosine phosphatases (PTPs). Here we report the characterization of cDNAs for two of the viral PTPs isolated by screening a cDNA library from haemocytes of parasitized host larvae. The two encoded proteins show 70% amino acid identity and are expressed in the fat body of parasitized hosts. In addition, one was expressed in inactivated prothoracic glands (PTGs), 24 h after parasitoid oviposition. The rapid block of ecdysteroidogenesis does not appear to be due to inhibition of general protein synthesis, as indirectly indicated by the unaltered S6 kinase activity in the cytosolic extracts of basal PTGs from parasitized host larvae. Rather, TnBV PTP over-expression in inactivated host PTGs suggests that gland function may be affected by the disruption of the phosphorylation balance of key proteins regulating points upstream from the ribosomal S6 phosphorylation in the PTTH signaling cascade.

Evolutionary mechanisms driving the evolution of a large polydnavirus gene family coding for protein tyrosine phosphatases

“…Some bracovirus PTP genes play an important role in host immune alteration particularly by modulating PTP cell activity in hemocytes [32]. They were also suggested to be involved in controlling larval development by acting on the level of phosphorylation of regulatory proteins involved in the prothoracic gland’s response to prothoracicotropic hormone (PTTH) required to produce ecdysteroids [65]. One particular class of PTPs has been identified for not carrying PTP activity, but the proteins were shown to reduce PTP cell activity probably through competition with host PTPs [32,34].…”

A transient increase in total head phosphotyrosine levels is observed upon the emergence of Aedes aegypti from the pupal stage

“…This injection impairs the development of the host larvae by altering the function of the prothoracic gland. The authors suggest that this mechanism is controlled by viralderived PTPs that protect the emerging parasite larvae against the host immune defences (Falabella et al 2006). The participation of PTPs has also been proposed for the enhanced locomotor activity of Baculovirus-infected B. mori larvae (Kamita et al 2005).…”

Polydnaviruses: From discovery to current insights

“…Several of these genes were also related to factors in eukaryotic signaling pathways, which suggested they were virulence factors that caused some of the physiological alterations that occur in parasitized hosts. Subsequent studies supported this by demonstrating experimentally how certain BV and IV gene products interact with host immune molecules or cells (Beck and Strand, 2005; Thoetkiattikul et al, 2005; Beck and Strand, 2007; Ibrahim and Kim, 2008; Labropoulou et al, 2008; Kwon and Kim, 2008; Cooper et al, 2011; Magkrioti et al, 2011; Bitra et al, 2012; Gueguen et al, 2013), while implicating other genes in altering host growth, metabolism or endocrine physiology (Provost et al, 2004; Falabella et al, 2006; Kim et al, 2013; Presad et al, 2013). …”