Literature DB >> 11961262

Characterization of two genes of the polydnavirus of Chelonus inanitus and their stage-specific expression in the host Spodoptera littoralis.

Andrea Johner1, Beatrice Lanzrein1.   

Abstract

Chelonus inanitus (Braconidae, Hymenoptera) is a solitary egg-larval parasitoid of Spodoptera littoralis. Along with the egg the female wasp injects polydnaviruses, which are prerequisites for successful parasitoid development. The polydnavirus genome is segmented and consists of double-stranded circular DNA. Proviral DNA is integrated in the wasp's genome; virus replication is restricted to the wasp's ovary and does not occur in the parasitized host. The polydnavirus of C. inanitus (CiV) protects the parasitoid larva from encapsulation by the host's immune system and causes a developmental arrest of the host in the prepupal stage. Here we report on the first two cloned CiV genes, which are named CiV14g1 and CiV14g2 because of their localization on segment CiV14. The cDNA of CiV14g1 has a size of 2036 bp; the gene contains seven exons interrupted by six introns of similar size and encodes a putative polypeptide of 548 amino acids. The cDNA of CiV14g2 has a size of 618 bp; the gene consists of three exons and encodes a putative peptide of 77 amino acids. Transcript quantities of both genes are very low up to the penultimate larval instar of the host. In the last instar, at the stage of pupal cell formation, CiV14g1 expression increases about 5-fold and CiV14g2 expression about a 1000-fold. These are the first data to show strong upregulation of polydnavirus genes towards the end of parasitization. These two genes might be involved in the reduction of host ecdysteroids observed at this stage.

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Year:  2002        PMID: 11961262     DOI: 10.1099/0022-1317-83-5-1075

Source DB:  PubMed          Journal:  J Gen Virol        ISSN: 0022-1317            Impact factor:   3.891


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6.  Role of Ovarian Proteins Secreted by Toxoneuron nigriceps (Viereck) (Hymenoptera, Braconidae) in the Early Suppression of Host Immune Response.

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