[Haploadaptivity of tumor suppressor lgl and ontogenesis in Drosophila melanogaster: increased survival rate and life span under stress conditions].

Mutations of tumor suppressor lgl induce neuroblastoma and malignant transformation of epithelial larval tissues in Drosophila. We have already shown that heterozygotes for lethal null variants lgl/+ are widespread in natural populations. In order to elucidate this paradox, we analyzed the parameters of biological adaptation of the carriers of one dose of the tumor suppressor. We studied the patterns of embryonic survival rate of lgl/+ flies under the conditions of competition for life resources and development at elevated and lowered temperatures (29 and 16 degrees C), influence of stress thermal conditions on life span, influence of short-term temperature stress during prezygotic period in the course of oogenesis of mothers on survival rate of F1 progenies, and resistance of heterozygotes for different lethal lgl alleles against RNA virus DCV. The loss of one dose of tumor suppressor lgl+ provided for increased survival rate and life span of lgl/+ heterozygotes under stress conditions. This phenomenon was called haploadaptivity. Important features of adaptogenesis were established in lgl/+ heterozygotes: dependence on the maternal genotype and critical periods in development. The increased survival rate of F1 progenies was determined already during early oogenesis of their lgl/+ mothers at the proembryo stage. With respect to humans, this conclusion draws attention to the oogenesis-dependent transgeneration aspect of determination and expression of mutant factors of risk, including tumor suppressors. The data obtained are essential for understanding of the causes of spreading null variants for the genes related to multiple pathologies, including cancer, in human populations.

Drosophila S virus, a hereditary reolike virus, probable agent of the morphological S character in Drosophila simulans.

Isometric reolike virions were found in all the examined Drosophila simulans flies from two strains (SimES-st and Israel-st) presenting the S phenotype, a maternally inherited morphological trait (abnormalities of bristles). Normal flies of both strains appeared virus-free. Virions were found in the cytoplasm of male and female gonads and epidermal cells, including the bristle-forming cells, which appeared disorganized. Steps of virogenesis were described. A positive correlation was demonstrated between expressivity of the S phenotype and degree of viral infection. This hereditary reolike virus seems to be responsible for the S character of D. simulans and was named DSV (Drosophila S virus).

Mutability studies in two Drosophila melanogaster isogenic stocks, endemic for C picornavirus and virus-free.

A virus-free Drosophila stock was obtained by outer disinfection of eggs from DCV-contaminated females. The healthy flies exhibited 3 times less lethal mutations on the X chromosome than did the diseased flies. In addition, on X and 2nd chromosomes, the mutability of the infected males was 2-3 times lower than that of the infected females. The natural viruses of Drosophila are partially responsible for the rate of mutations occurring in the wild populations of this insect.

The proteins expressed by different isolates of Drosophila C virus.

Isolates of Drosophila C virus (DCV) from Drosophila flies obtained in geographically different regions were adapted to growth in Drosophila tissue culture cells. The viruses, purified from tissue culture cells, were shown to be serologically related to one of the isolates ("O" from Ouarzazate, Morocco). Analysis of the structural proteins by polyacrylamide gel electrophoresis demonstrated differences between the isolates. Labelling intracellular proteins of infected Drosophila melanogaster cells with 35S-methionine at 28 degrees C demonstrated the presence of the virus structural proteins and their immediate precursors. Raising the temperature to 37 degrees C both before and during the pulse period inhibited the processing of the high molecular weight proteins and resulted in a greater "shut-off" of host cell proteins than viral induced proteins. This allowed the precursor proteins to be compared as well as the structural proteins of the different strains. It was possible to clearly distinguish differences between the isolates on the basis of the induced proteins, although limited proteolysis of corresponding proteins showed marked similarities. Hence it is possible to distinguish between different isolates of the "same" small RNA-virus of insects from geographically different regions.

The polypeptides induced in Drosophila cells by Drosophila C virus (strain Ouarzazate).

The Ouarzazate strain of Drosophila virus (DCV0) was grown in Drosophila melanogaster tissue culture cells, and [35S]methionine-labeled virions were found to contain a group of major structural proteins with a molecular weight of approximately 30,000 as well as several minor proteins of higher molecular weight and a protein of approximately 10,000 daltons. Using a range of pulses, chases and gel systems, examination of the intracellular proteins induced by DCV0 showed the presence of 17 polypeptides not found in uninfected cells. The synthesis of virus-induced polypeptides was extremely asymmetric with a rapid appearance of the major virus structural proteins and a much slower appearance of the lowest molecular weight structural protein (VP4). Processing of virus-induced proteins including the appearance of VP4 was demonstrated using pulse-chase after pulsing with [35S]methionine. While the highest molecular weight induced protein found in infected cells was 146,000, pretreatment of cells with iodoacetamide resulted in the appearance of a protein with a molecular weight of approximately 200,000. The evidence presented in this paper supports the inclusion of DCV0 in the Picornaviridae group.

Drosophila melanogaster as an experimental host for study of multiplication and biology of the mycoplasma inducing the "lethargy of coleoptera".

The mulitplication of the mycoplasma responsible for the "lethargy of coleoptera" on a laboratory host, Drosophila melanogaster, was obtained on the first passage. Independant series of successive passages on D. melanogaster were performed without any apparent modifications of the properties of the microorganism. Pathogenicity for its natural host Melolontha melolontha was retained. The different forms of mycoplasma observed lead us to propose a probable cycle of development, composed of a succession of globular and rod-shaped bodies, these later being often sinuous. The infected Drosophila flies presented a reduced life span and fertility. Infection of the cephalic nervous system seems to be responsible for death. Horizontal transmission of the microorganism was not observed.

A comparison of buoyant density and polypeptides of Drosophila P, C and A viruses.

On the basis of their buoyant densities in CsCl and their capsid polypeptides, three viruses isolated from Drosophila spp. which were originally described as serotypes, are now classified as distinct viruses. The biochemical properties of each virus suggest that it has several key features in common with the mammalian picornaviruses.

[Study of the vertical transmission and horizontal transmission of "Drosophila melanogaster" and "Drosophila immigrans" picornavirus (author's transl)]. / Etude de la transmission horizontale et de la transmission verticale des picornavirus de Drosophilia melanogaster et de Drosophila immigrans

The contamination of drosophila eggs, of larvae of the 3 instars and of adults, was studied using several strains of P and C viruses of D. melanogaster and of iota virus of D. immigrans. The infected adults contaminated other flies if they were rich in viral particles and if the contact was long enough. Infection of the adults occurred in the presence of concentrated viral suspensions. The larvae were easily infected when they grew in contaminated media; the more sensitive stage was the first instar. Transovarian transmission was observed only in naturally infected flies propagating viruses of serotype I or III. C viruses were not hereditarily transmitted. Persistence of the Picornaviruses of drosophila populations can be explained by the additive effects of the 3 mechanisms of contamination.

[The discovery, in Drosophila, of viruses belonging to three new groups]. / Découverte, chez la Drosophile, de virus appartenant à trois nouveaux groupes

Viruses belonging to three new groups have been discovered by the technique used to detect the Picornaviruses. Virus F was found in two French laboratory stocks of D. melanogaster. Virus G and virus RS came from wild flies: a sample of D. melanogaster from Guiana (virus G) and a mixture of different Drosophila species from Singapore (virus G and virus RS).

Picornaviruses of laboratory and wild Drosophila melanogaster: geographical distribution and serotypic composition.

Picornaviruses were sought in a large number of D. melanogaster strains, coming from laboratories or recently collected from different parts of the world. About a third of these stocks contained viruses. Regions naturally infected were warm countries. Picornaviruses found in laboratories as well as in wild drosophila flies were the already known P and C viruses, of serotype 1 and 2, and a new virus of serotype 3 belonging by its biological properties to the P group. We did not find derological relationship between D. melanogaster and A. mellifera Picornaviruses.