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Venom of the parasitoid wasp Nasonia vitripennis changes the metabolism and gene expression in its fly host Sarcophaga bullata to induce developmental arrest, suppression of the immune response and various other venom effects. Yet, the venom of ectoparasitoid wasps has not been fully characterized. A major component of N. vitripennis venom is an uncharacterized, high-expressing protein referred to as Venom Y. Here we describe the evolutionary history and possible functions of this venom protein. We found that Venom Y is a relatively young gene that has duplicated to form two distinct paralogue groups. A copy of Venom Y has been recruited as a venom protein in at least five wasp species. Functional analysis found that Venom Y affects detoxification and immunity genes in envenomated fly hosts. Many of these genes are fat-body specific, suggesting that Venom Y may have a targeted effect on fat body tissue. We also show that Venom Y may mitigate negative effects of other venom proteins. Finally, protein sequencing indicates that Venom Y is post-translationally modified. This study contributes to elucidating parasitoid venom by using RNA interference knockdown to investigate venom protein function in the context of the whole venom cocktail., (© 2019 The Royal Entomological Society.)

Venom from the parasitoid wasp Nasonia vitripennis dramatically elevates sorbitol levels in its natural fly hosts. In humans, sorbitol elevation is associated with complications of diabetes. Here we demonstrate that venom also induces this disease-relevant phenotype in human cells, and investigate possible pathways involved. Key findings are that (a) low doses of Nasonia venom elevate sorbitol levels in human renal mesangial cells (HRMCs) without changing glucose or fructose levels; (b) venom is a much more potent inducer of sorbitol elevation than glucose; (c) low venom doses significantly alter expression of genes involved in sterol and alcohol metabolism, transcriptional regulation, and chemical/stimulus response; (d) although venom treatment does not alter expression of the key sorbitol pathway gene aldose reductase (AR); (e) venom elevates expression of a related gene implicated in diabetes complications (AKR1C3) as well as the fructose metabolic gene (GFPT2). Although elevated sorbitol is accepted as a major contributor to secondary complications of diabetes, the molecular mechanism of sorbitol regulation and its contribution to diabetes complications are not fully understood. Our findings suggest that genes other than AR could contribute to sorbitol regulation, and more broadly illustrate the potential of parasitoid venoms for medical application., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

We report here a cytogenetic and molecular analysis of two cases of T-cell leukemia with t(14;14) (q11.2;q32). Through in situ hybridization and Southern blotting, using radioactively labeled immunoglobulin heavy chain (IGH) and alpha T-cell receptor (TCRA) gene probes, we found in both tumors that the loci of both IGH and TCRA were rearranged. Molecular analysis of the t(14;14) clearly demonstrated that in some tumors rearrangements of the IGH and TCRA genes are associated with interchromosomal exchanges that result in specific chromosome translocations that confer a proliferative advantage and predisposition to leukemic transformation. The implication of these rearrangements for normal and neoplastic T-cell development is discussed.

Retinoblastoma (Rb) cells may be more sensitive to X-irradiation than normal cells when assayed for clonogenic survival, suggesting that such sensitivity can be used as a trait for detecting RB1 gene carriers. We studied induction of chromosome damage in lymphocytes from patients with Rb by the radiomimetic antineoplastic antibiotic, bleomycin (BL). Lymphocytes were treated in G2 for 4 h at four concentrations of the drug (0.0, 0.3, 0.9, and 2.7 micrograms/ml), and chromosome damage was evaluated. No difference in levels of spontaneous or induced damage was detected among hereditary Rb, non-hereditary Rb, and normal lymphocytes. The role of X-ray treatment in the induction of second tumors in Rb patients is discussed.

A TL+ leukemia of a (B6 X A)F1 hybrid mouse (H-2b/H-2a) was previously subjected to immunoselection against H-2a by passage in (B6 X A.SW)F1 mice (H-2b/H-2s). A variant leukemia line was obtained that serologically lacked not only the H-2a phenotype but also the TL phenotype determined by the linked cis Tlaa allele of strain A. The H-2b phenotype and the TL phenotype of the Tlab allele of the B6 strain, which is expressed only by leukemia cells, were retained by the variant. Southern blotting with an H-2 cDNA probe that identifies restriction fragment polymorphisms distinguishing alleles of the H-2 and Tla regions of the B6 and A strains indicates that both the H-2a and Tlaa alleles are missing from the genome of this H-2a:Tlaa negative variant. Since the variant has two apparently unaltered chromosomes 17, where the H-2:Tla complex is situated, and since the intensity of bands in Southern blotting is suggestive of H-2b homozygosity, it is considered that loss of the H-2a:Tlaa haplotype by the variant was accompanied by duplication of the H-2b:Tlab haplotype. The implied change from heterozygosity to homozygosity that the variant has undergone with respect to H-2:Tla was not paralleled by a similar change at the three other loci tested, since the variant retained heterozygosity for Pep-3 (chromosome 1), Gpi-1 (chromosome 7), and Es-1 (chromosome 8).