Heritable Melanism and Parasitic Infection Both Result in Black-Spotted Mosquitofish

Male Gambusia holbrooki (Eastern Mosquitofish) express a heritable pigmentation polymorphism: ≈99% of males are silver, and only ≈1% have a melanic, black-spotted pattern. Sex-linkage, an autosomal modifier, and temperature control the expression of this heritable melanism. In many teleosts, melanin also accumulates around the site of parasitic invasion. We have identified black-spot disease in wild mosquitofish from their native habitat. Here, we demonstrate convergence upon the black-pigmented phenotype through two means: 1) heritable melanism, and 2) melanic spotting on the silver genotype that results from infection with immature encysted trematodes. Females are silver and express greater avoidance ofmelanic males during mating attempts. The resemblance of the black-spotted pattern of the melanic genotype to that of silver genotype infected with trematodes may affect the fitness ofmelanic males if females perceive them as diseased. Alternatively, females may shun parasitized silverfish because they resemble the melanic genotype, which is larger and has a larger mating orga

FOXO Regulates Organ-Specific Phenotypic Plasticity In Drosophila

Phenotypic plasticity, the ability for a single genotype to generate different phenotypes in response to environmental conditions, is biologically ubiquitous, and yet almost nothing is known of the developmental mechanisms that regulate the extent of a plastic response. In particular, it is unclear why some traits or individuals are highly sensitive to an environmental variable while other traits or individuals are less so. Here we elucidate the developmental mechanisms that regulate the expression of a particularly important form of phenotypic plasticity: the effect of developmental nutrition on organ size. In all animals, developmental nutrition is signaled to growing organs via the insulin-signaling pathway. Drosophila organs differ in their size response to developmental nutrition and this reflects differences in organ-specific insulin-sensitivity. We show that this variation in insulin-sensitivity is regulated at the level of the forkhead transcription factor FOXO, a negative growth regulator that is activated when nutrition and insulin signaling are low. Individual organs appear to attenuate growth suppression in response to low nutrition through an organ-specific reduction in FOXO expression, thereby reducing their nutritional plasticity. We show that FOXO expression is necessary to maintain organ-specific differences in nutritional-plasticity and insulin-sensitivity, while organ-autonomous changes in FOXO expression are sufficient to autonomously alter an organ's nutritional-plasticity and insulin-sensitivity. These data identify a gene (FOXO) that modulates a plastic response through variation in its expression. FOXO is recognized as a key player in the response of size, immunity, and longevity to changes in developmental nutrition, stress, and oxygen levels. FOXO may therefore act as a more general regulator of plasticity. These data indicate that the extent of phenotypic plasticity may be modified by changes in the expression of genes involved in signaling environmental information to developmental processes

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Oncoselective Parvoviral Vector-Mediated Gene Therapy of Cancer

We replaced capsid genes by reporter genes and assessed expression in different types of human cancer cells and their normal counterparts, either at the level of whole cell population (CAT ELISA) or at the single cell level [FACS analysis of green fluorescent protein (GFP)]. CAT expression was substantial (up to 10,000 times background) in all infected tumor cells, despite variations according to the cell types. In contrast, no gene expression was detected in similarly infected normal cells (with the exception of an expression slightly above background in fibroblasts). FACS analysis of GFP expression revealed that most tumor cells expressed high level of GFP while no GFP-positive normal cells could be detected with the exception of very few (less than 0.1%) human fibroblast cells expressing high level of GFP. We also replace capsid genes by genes coding for the costimulatory molecules B7-1 and B7-2 and show that, upon infection with B7 recombinant virions, only tumor cells display the costimulatory molecules and their immunogenicity was increased without any effect on normal cells. Using a recombinant minute virus of mice (MVM) containing the herpes simplex thymidine kinase gene, we could get efficient killing of most tumor cell types in the presence of ganciclovir, without affecting normal proliferating cells. The prospects and limitations of these different strategies are discussed.SCOPUS: cp.jinfo:eu-repo/semantics/publishe

Oncoselective transduction of CD80 and CD86 in tumor cell lines using an autonomous recombinant parvovirus.

BACKGROUND: The aim of this study was to enhance selectively the immunostimulatory properties of tumor cells. Based on their oncotropic properties, we used autonomous recombinant parvoviruses to transduce the genes coding for the constimulatory molecules CD80 (B7-1) or CD86 (B7-2) specifically into tumor cells without transducing normal cells. MATERIALS AND METHODS: After infection of tumor cells by these viruses, surface expression of CD80 and CD86 molecules was assessed by FACS and enhancement of immunostimulatory properties was assessed in alloreactions with G-10 purified T cells. RESULTS: Infection of normal and transformed cells with recombinant MVM- B7-1 or B7-2 viruses leads to expression of costimulatory molecules only by tumor cells and confers on them the capacity to sensitize naive T cells in vitro. CONCLUSION: This approach should ultimately lead to selective expression of costimulatory molecules in tumor tissues in vivo without affecting normal cells.Journal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe