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S Ronsseray

Publications and source records attributed to S Ronsseray.

17 recordsLinked to original sources
PubMed2004

aubergine mutations in Drosophila melanogaster impair P cytotype determination by telomeric P elements inserted in heterochromatin.

Transposable P elements inserted in the heterochromatic Telomeric Associated Sequences on the X chromosome (1A site) of Drosophila melanogaster have a very strong capacity to elicit the P cytotype, a maternally transmitted condition which represses P element transposition and P-induced hybrid dysgenesis. This repressive capacity has previously been shown to be sensitive to mutant alleles of the gene Su(var)205, which encodes HP1 (Heterochromatin Protein 1), thus suggesting a role for chromatin structure in repression. Since an interaction between heterochromatin formation and RNA interference has been reported in various organisms, we tested the effect of mutant alleles of aubergine, a gene that has been shown to play a role in RNA interference in Drosophila, on the repressive properties of telomeric P elements. Seven out of the eight mutant alleles tested clearly impaired the repressive capacities of the two independent telomeric P insertions at 1A analyzed. P repression by P strains whose repressive capacities are not linked to the presence of P copies at 1A were previously found to be insensitive to Su(var)205; here, we show that they are also insensitive to aubergine mutations. These results strongly suggest that both RNA interference and heterochromatin structure are involved in the establishment of the P cytotype elicited by telomeric P elements, and reinforce the hypothesis that different mechanisms for repression of P elements exist which depend on the chromosomal location of the regulatory copies of P.

Alleles↗
PubMed2002

P element-encoded regulatory products enhance Repeat-Induced Gene Silencing (RIGS) of P-lacZ-white clusters in Drosophila melanogaster.

In Drosophila melanogaster, some clusters of P transgenes ( P-lacZ-white) display a variegating phenotype for the white marker in the eye, a phenomenon termed "Repeat-Induced Gene Silencing" (RIGS). We have tested the influence of the P element repression state (P cytotype) on the eye phenotype of several P-lac-w clusters that differ in transgene copy number or genomic insertion site. P element-encoded regulatory products strongly enhance RIGS. The effect occurs in both sexes, is detectable with clusters having at least three copies and is observed at both genomic locations tested (cytogenetic regions 50C and 92E). Single variegating P-lac-w transgenes located in pericentromeric heterochromatin are not affected by P regulatory products. All P strain backgrounds tested enhance RIGS, including chromosomes bearing a single P element encoding a truncated P transposase or carrying a single internally deleted KP element. Therefore, clusters are highly sensitive to different types of P repressors. Finally, a chimeric gene in which the 5' portion of the P element is fused to the polyhomeotic coding sequence (ph(p1)) also strongly enhances silencing of P-lac-w clusters. These results have implications for the mechanism of action of the P repressors and show that P transgene clusters represent a new class of P-sensitive alleles, providing a simple assay for somatic P repression that can be completed in one generation.

ATP-Binding Cassette Transporters↗
PubMed2001

P-Element repression in Drosophila melanogaster by variegating clusters of P-lacZ-white transgenes.

In Drosophila, clusters of P transgenes (P-lac-w) display a variegating phenotype for the w marker. In addition, X-ray-induced rearrangements of chromosomes bearing such clusters may lead to enhancement of the variegated phenotype. Since P-lacZ transgenes in subtelomeric heterochromatin have some P-element repression abilities, we tested whether P-lac-w clusters also have the capacity to repress P-element activity in the germline. One cluster (T-1), located on a rearranged chromosome (T2;3) and derived from a line bearing a variegating tandem array of seven P-lac-w elements, partially represses the dysgenic sterility (GD sterility) induced by P elements. This cluster also strongly represses in trans the expression of P-lacZ elements in the germline. This latter suppression shows a maternal effect. Finally, the combination of variegating P-lac-w clusters and a single P-lacZ reporter inserted in subtelomeric heterochromatic sequences at the X chromosome telomere (cytological site 1A) leads to strong repression of dysgenic sterility. These results show that repression of P-induced dysgenic sterility can be elicited in the absence of P elements encoding a polypeptide repressor and that a transgene cluster can repress the expression of a single homologous transgene at a nonallelic position. Implications for models of transposable element silencing are discussed.

ATP-Binding Cassette Transporters↗
PubMed2000

P-Element repression in Drosophila melanogaster by a naturally occurring defective telomeric P copy.

In Drosophila melanogaster, hybrid dysgenesis occurs in progeny from crosses between females lacking P elements and males carrying P elements scattered throughout the genome. We have genetically isolated a naturally occurring P insertion at cytological location 1A, from a Tunisian population. The Nasr'Allah-P(1A) element [NA-P(1A)] has a deletion of the first 871 bp including the P promoter. It is flanked at the 3' end by telomeric associated sequences and at the 5' end by a HeT-A element sequence. The NA-P(1A) element strongly represses dysgenic sterility and P transposition. However, when testing P-promoter repression, NA-P(1A) was unable to repress a germinally expressed P-lacZ construct bearing no 5'-homology with it. Conversely, a second P-lacZ construct, in which the fusion with lacZ takes place in exon 3 of P, was successfully repressed by NA-P(1A). This suggests that NA-P(1A) repression involves a homology-dependent component.

Alleles↗
PubMed1998

Repression of hybrid dysgenesis in Drosophila melanogaster by combinations of telomeric P-element reporters and naturally occurring P elements.

In Drosophila melanogaster, hybrid dysgenesis occurs in the germline of flies produced by crosses between females lacking P elements and males carrying 25-55 P elements. We have previously shown that a complete maternally inherited repression of P transposition in the germline (P cytotype) can be elicited by only two autonomous P elements located at the X chromosome telomere (cytological site 1A). We have tested whether P transgenes at 1A, unable to code for a P-repressor, may contribute to the repression of P elements. Females carrying a P-lacZ transgene at 1A ["P-lacZ(1A)"], crossed with P males, do not repress dysgenic sterility in their progeny. However, these P-lacZ(1A) insertions, maternally or paternally inherited, contribute to P-element repression when they are combined with other regulatory P elements. This combination effect is not seen when the P-lacZ transgene is located in pericentromeric heterochromatin or in euchromatin; however a P-w,ry transgene located at the 3R chromosome telomere exhibits the combination effect. The combination effect with the P-lacZ(1A) transgene is impaired by a mutant Su(var)205 allele known to impair the repression ability of the autonomous P elements at 1A. We hypothesized that the combination effect is due to modification of the chromatin structure or nuclear location of genomic P elements.

Animals↗
PubMed1997

P element regulation and X-chromosome subtelomeric heterochromatin in Drosophila melanogaster.

In Drosophila melanogaster, crossing males carrying autonomous P elements with females devoid of P copies results in hybrid dysgenesis in the germline of progeny. The reciprocal cross produces non-dysgenic progeny due to a maternally inherited state non-permissive for P transposition. The capacity of a P copy to repress transposition depends on both its structure and its chromosomal location. Naturally occurring regulatory P elements inserted at the telomere of the X chromosome have been genetically isolated in a genomic context devoid of other P elements. One or two copies of autonomous P elements at this site (1A) are sufficient to elicit a strong P repression in the germline. These elements are flanked by Telomeric Associated Sequences, previously identified and described by Karpen and Spradling (1992) as having heterochromatic properties. The regulatory properties of P elements at 1A are strongly impaired by mutations affecting Su(var)205, which encodes Heterochromatin Protein 1, a non-histone heterochromatin protein. The regulatory properties of classical P strains are not sensitive to Su(var)205. Models based on chromatin structure or on nuclear localisation of the telomeres are discussed in order to explain both the strong regulatory properties of P elements at the X chromosome telomere and their sensitivity to Su(var)205.

Animals↗
PubMed1996

The regulatory properties of autonomous subtelomeric P elements are sensitive to a Suppressor of variegation in Drosophila melanogaster.

Genetic recombination was used in Drosophila melanogaster to isolate P elements, inserted at the telomeres of X chromosomes (cytological site IA) from natural populations, in a genetic background devoid of other P elements. We show that complete maternally inherited P repression in the germline (P cytotype) can be elicited by only two autonomous P elements at 1A and that a single element at this site has partial regulatory properties. The analysis of the surrounding chromosomal regions of the P elements at 1A shows that in all cases these elements are flanked by Telomeric Associated Sequences, tandemly repetitive noncoding sequences that have properties of heterochromatin. In addition, we show that the regulatory properties of P elements at 1A can be inhibited by some of the mutant alleles of the Su(var)205 gene and by a deficiency of this gene. However, the regulatory properties of reference P strains (Harwich and Texas 007) are not impaired by Su(var)205 mutations. Su(var)205 encodes Heterochromatin Protein 1 (HP1). These results suggest that the HP1 dosage effect on the P element properties is site-dependent and could involve the structure of the chromatin.

Animals↗
PubMed1993

Maternal inheritance of P cytotype in Drosophila melanogaster: a "pre-P cytotype" is strictly extra-chromosomally transmitted.

In Drosophila melanogaster, transposition of the P element is under the control of a cellular state known as cytotype. The P cytotype represses P transposition whereas the M cytotype is permissive for transposition. In the long-term, the P cytotype is determined by chromosomal P elements but over a small number of generations it is maternally inherited. In order to analyse the nature of this maternal inheritance, we tested whether a maternal component can be transmitted without chromosomal P elements. We used a stable determinant of P cytotype, linked to the presence of two P elements at the tip of the X chromosome (1A site) in a genome devoid of other P elements. We measured P repression capacity using two different assays: gonadal dysgenic sterility (GD) and P-lacZ transgene repression. We show that zygotes derived from a P cytotype female (heterozygous for P (1A)/balancer devoid of P copies) and which inherit no chromosomal P elements from the mother, have, however, maternally received a P-type extra-chromosomal component: this component is insufficient to specify the P cytotype if the zygote formed does not carry chromosomal P elements but can promote P cytotype determination if regulatory P elements have been introduced paternally. We refer to this strictly extra-chromosomally inherited state as the "pre-P cytotype". In addition, we show that a zygote that has the pre-P cytotype but which has not inherited any chromosomal P elements, does not transmit the pre-P cytotype to the following generation. The nature of the molecular determinants of the pre-P cytotype is discussed.

Animals↗
PubMed1993

Maternal repression of the P element promoter in the germline of Drosophila melanogaster: a model for the P cytotype.

The transposition of P elements in Drosophila melanogaster is regulated by products encoded by the P elements themselves. The P cytotype, which represses transposition and associated phenomena, exhibits both a maternal effect and maternal inheritance. The genetic and molecular mechanisms of this regulation are complex and not yet fully understood. In a previous study, using P-lacZ fusion genes, we have shown that P element regulatory products were able to inhibit the activity of the P promoter in somatic tissues. However, the repression observed did not exhibit the maternal effect characteristic of the P cytotype. With a similar approach, we have assayed in vivo the effect of P element regulatory products in the germline. We show that the P cytotype is able to repress the P promoter in the germline as well as in the soma. Furthermore, this repression exhibits a maternal effect restricted to the germline. On the basis of these new observations, we propose a model for the mechanism of P cytotype repression and its maternal inheritance.

Animals↗
PubMed1993

Distribution and conservation of sequences homologous to the 1731 retrotransposon in Drosophila.

The distribution of 1731 retrotransposon-hybridizing sequences in the family Drosophilidae has been studied using a 1731 probe from Drosophila melanogaster. Squash blot and Southern blot analyses of 42 species reveal that the 1731 sequences are widespread within both the Sophophora and Drosophila subgenera and are also present in the genera Scaptomyza and Zaprionus. Hence the 1731 retrotransposon family appears to have a long evolutionary history in the Drosophilidae genome. Differences of hybridization signal intensity suggested that the 1731 sequence is well conserved only in the three species most closely related to D. melanogaster (D. simulans, D. mauritiana, and D. sechellia). A survey of insertion sites in numerous different populations of the previous four species by in situ hybridization to polytene chromosomes has shown in all cases both chromocentric hybridizations and a low number of sites (0-5) on the chromosomal arms. This number of sites is among the lowest observed in D. melanogaster and D. simulans when 1731 is compared with other retrotransposon families. In addition, we have observed species-specific patterns of the chromocentric hybridization signal, suggesting rapid modifications of the beta-heterochromatin components since the radiation of the melanogaster subgroup.

Animals↗
PubMed1991

The maternally inherited regulation of P elements in Drosophila melanogaster can be elicited by two P copies at cytological site 1A on the X chromosome.

Two P elements, inserted at the cytological site 1A on an X chromosome from an Drosophila melanogaster natural population (Lerik, USSR), were isolated by genetic methods to determine if they are sufficient to cause the P cytotype, the cellular condition that regulates the P family of transposable element. The resulting "Lerik P(1A)" line (abbreviated "Lk-P(1A)") carries only one P element in situ hybridization site but genomic Southern analysis indicates that this site contains two, probably full length, P copies separated by at least one EcoRI cleavage site. Because the Lk-P(1A) line shows some transposase activity, at least one of these two P elements is autonomous. The Lk-P(1A) line fully represses germline P element activity as judged by the GD sterility and snw hypermutability assays; this result shows that the P cytotype can be elicited by only two P element copies. However, the Lk-P(1A) line does not fully repress delta 2-3(99B) transposase activity in the soma, although it fully represses delta 2-3(99B) transposase activity in the germline (delta 2-3(99B) is an in vitro modified P element that produces a high level of transposase activity in both the germline and the soma). The germline regulatory properties of the Lk-P(1A) line are maternally transmitted, even when the delta 2-3(99B) element is used as the source of transposase. By contrast, the partial regulation of delta 2-3(99B) somatic activity is chromosomally inherited. These results suggest that the regulatory P elements of the Lk-P(1A) line are inserted near a germline-specific enhancer.

Animals↗
PubMed1990

Localization of P elements, copy number regulation, and cytotype determination in Drosophila melanogaster.

Seventeen highly-inbred lines of Drosophila melanogaster extracted from an M' strain (in the P/M system of hybrid dysgenesis) were studied for their cytotype and the number and chromosomal location of complete and defective P elements. While most lines were of M cytotype, three presented a P cytotype (the condition that represses P-element activity) and one was intermediate between M and P. All lines were found to possess KP elements and only eight to bear full-sized P elements. Only the lines with full-sized P elements showed detectable changes in their P-insertion pattern over generations; their rates of gain and of loss of P-element sites were equal to 0.12 and 0.09 per genome, per generation, respectively. There was no correlation between these two rates within lines, suggesting independent transpositions and excisions in the inbred genomes. The results of both Southern blot analysis and in situ hybridization of probes made from left and right sides of the P element strongly suggested the presence of a putative complete P element in region 1A of the X chromosome in the three lines with a P cytotype; the absence of P copy in this 1A region in lines with an M cytotype, favours the hypothesis that the P element inserted in 1A could play a major role in the P-cytotype determination. Insertion of a defective 2 kb P element was also observed in region 93F in 9 of the 13 M lines. The regulation of the P-element copy number in our lines appeared not to be associated with the ratio of full-length and defective P elements.

Animals↗
PubMed1989

Copy number and distribution of P and I mobile elements in Drosophila melanogaster populations.

The distribution of the number of copies of P and I transposable elements per genome was investigated by in situ hybridization for a large set of Drosophila melanogaster strains. These included the P, Q and M' types of the P-M system of hybrid dysgenesis. P element copy number varied widely (range 5-59). P and Q strains had around 40 copies whereas M' strains generally had lower numbers (between 5 and 35) with one extreme value (52). The copy number of I elements appeared to be precisely regulated, as no strains were found outside the 15 +/- 5 range. The number of copies of the two families were independent. An excess of P copies on the X chromosome compared with the autosomes was found for the P and Q strains, but not for M' strains. Among X-inserted P sites, a very high frequency of occupation was found at the tip of the X chromosome (cytological site 1A), especially for P and Q strains. The possible regulatory role in the P-M system of X-inserted P sites is discussed.

Animals↗
PubMed1989

Comparison of the regulation of P elements in M and M' strains of Drosophila melanogaster.

M and M' strains of Drosophila melanogaster in the P-M system of hybrid dysgenesis were compared in two series of tests, with the following results. (1) The singed-weak hypermutability regulation test showed that M' strains had lower P excision rates than M strains, suggesting that P-elements repression must occur in M' strains although it is not detectable by gonadal dysgenesis assays. (2) The evolution of mixed P+M and mixed P+M' populations was compared, using a strong P strain. The P+M cultures invariably evolved in a few generations into strong P cultures, while the P+M' cultures evolved into P-type cultures with reduced P-factor potentials. However, after 30 generations of culture, both these types of mixed cultures had similar P copy numbers, suggesting that regulation of copy number had occurred in them.

Animals↗
PubMed1989

Are Drosophila melanogaster populations under a stable geographical differentiation due to the presence of P elements?

In order to simulate the outcome of the P-M status of Eurasian populations of Drosophila melanogaster, the evolution of experimental mixed-strains was monitored for up to 50 generations. The results were compared with the evolution in natura of European populations sampled in 1981-83 and 1986-87 over a similar period of time. Different combinations of P and M' strains, Q and M' strains, M' and M' strains and M and M' strains were set up at 25 degrees C and duplicated at 13 degrees C night-21 degrees C day. The possibility of a change towards a P type only appeared with the introduction of the strong P strain Harwich into Eurasian strains. Strains with strength similar to that of Harwich are not currently found in wild populations. With the introduction of weak P and Q strains of the strength presently observed in western Europe, experimental populations evolved slowly towards a Q state or a weak M' state. M'-M' mixed populations resulted in strong M' strains, as was the case for M-M' populations. In these cases. P sequences were not eliminated. In wild populations both genetic and molecular analyses showed no significant differences, over a five year period, for GD sterility potentials, for total P copy number or for distribution of the full-sized and KP elements. Changes in Eurasian populations are probably taking place at a very low rate and may even have stopped, leading to a quasi-stable differentiation over the continent. During the different steps of progressive invasion of P transposable elements, several deleted elements developed and natural selection may have acted on them. The possibility of the selection of different types of regulatory mechanisms according to the presence of different kinds of derivative elements, leading to a world-wide differentiation between P-Q and M' strains is discussed.

Animals↗
PubMed1984

Hybrid dysgenesis in Drosophila melanogaster: influence of temperature on cytotype determination in the P-M system.

In Drosophila melanogaster, the P-M system of hybrid dysgenesis is a syndrome of germ line abnormalities, including temperature dependent gonadal dysgenesis (GD sterility), high rates of mutation and male recombination, which occurs in some interstrain hybrids but only from one of the two crosses. In the P-M system, hybrid dysgenesis results from interaction between chromosomally transposable elements of the P element family and a particular extrachromosomal state referred to as the M cytotype. Cytotype (M or P) is known to be determined by the absence or presence of chromosomal factors, but principally with limited cytoplasmic transmission. In a series of experiments in which F1 hybrid females from various P and M strains were submitted to different preadult and ageing temperature treatments, it was found that the cytotype switch is strongly temperature-dependent in the F1 females from M female X P male but not in the reciprocal cross. In the F1 females from the former cross, a strong M cytotype occurs at a low developmental temperature (18 degrees C) and a weak M cytotype occurs at a high developmental temperature (26.5 degrees C). On the other hand, a high ageing temperature applied after a low developmental temperature switches the cytotype from M to P and reciprocally, a low ageing temperature applied after a high developmental temperature switches the cytotype from P to M.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗