scholarly journals 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.

Genetics ◽  
1991 ◽  
Vol 129 (2) ◽  
pp. 501-512 ◽  
Author(s):  
S Ronsseray ◽  
M Lehmann ◽  
D Anxolabéhère

Abstract 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.

1990 ◽  
Vol 56 (1) ◽  
pp. 3-14 ◽  
Author(s):  
C. Biémont ◽  
S. Ronsseray ◽  
D. Anxolabéhère ◽  
H. Izaabel ◽  
C. Gautier

SummarySeventeen 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 K.P 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.


Genetics ◽  
2001 ◽  
Vol 159 (4) ◽  
pp. 1631-1642 ◽  
Author(s):  
Stéphane Ronsseray ◽  
Antoine Boivin ◽  
Dominique Anxolabéhère

Abstract 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.


Genetics ◽  
1996 ◽  
Vol 143 (4) ◽  
pp. 1663-1674 ◽  
Author(s):  
Stéphane Ronsseray ◽  
Monique Lehmann ◽  
Danielle Nouaud ◽  
Dominique Anxolabéhère

Abstract Genetic recombination was used in Drosophila melanogaster to isolate P elements, inserted at the telomeres of X chromosomes (cytological site 1A) 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 sitedependent and could involve the structure of the chromatin.


1992 ◽  
Vol 60 (3) ◽  
pp. 165-174
Author(s):  
P. Eggleston ◽  
K. A. Exley

SummaryThe frequency, distribution and structure of P elements on the second and third chromosomes of Texas 1, a wild-type inbred strain of Drosophila melanogaster, were investigated by in situ hybridization. These autosomes were isolated individually and used as P-element donors to study the frequency and distribution of male recombination events generated on recipient chromosomes which were originally devoid of P sequences. The P-element array of chromosome 2 was shown to generate higher male recombination frequencies on chromosome 3 than vice versa, despite having fewer P factors and fewer P elements in general. This is likely to be due to the presence and distribution of specific P-deletion derivatives, which vary in their ability to repress P mobility. The male recombination generated on recipient chromosomes is associated with the insertion of donated P sequences, but only in a small minority of cases could a novel P-element site be detected at, or near, the recombination breakpoint. The majority of such breakpoints appear to be associated either with unsuccessful P insertion, or with the action of P transposase attracted by P elements newly inserted elsewhere on the recipient chromosome. Recent evidence also suggests that a small proportion of the breakpoints may be associated with the action of P transposase alone. Male recombination breakpoints appear to be distributed effectively at random along the recipient autosomes, and their frequency of occurrence was shown to correlate with the physical length of DNA available between markers, as revealed by the polytene map distance.


Genetics ◽  
1990 ◽  
Vol 124 (2) ◽  
pp. 331-337 ◽  
Author(s):  
J A Sved ◽  
W B Eggleston ◽  
W R Engels

Abstract The P element insertion delta 2-3(99B) has previously been shown to activate incomplete P elements elsewhere in the genome. We show that this element, in conjunction with a second incomplete P element, P[CaSpeR], also induces recombination in the male germ line. The recombination is induced preferentially in the region of the P[CaSpeR] element. Recombinant chromosomes contain the P[CaSpeR] element in more than 50% of cases, and alternative models of transposon replication and preferential chromosome breakage are put forward to explain this finding. As is the case with male recombination induced by P-M dysgenic crosses, recombination appears to be premeiotic in a high proportion of cases. The delta 2-3(99B) element is known to act in somatic cells. Correspondingly, we show that the delta 2-3(99B)-P[CaSpeR] combination elevates the incidence of somatic recombination.


1991 ◽  
Vol 57 (3) ◽  
pp. 213-226 ◽  
Author(s):  
Ellen M. Heath ◽  
Michael J. Simmons

SummaryTwelve inbred lines derived from an M′ strain of Drosophila melanogaster were used to study the repression of P-element-mediated hybrid dysgenesis. Initial assessments indicated that the lines differed in the ability to repress gonadal dysgenesis, and that this ability was highly correlated with the ability to repress snw hypermutability. Later assessments indicated that most of the lines with low or intermediate repression potential evolved to a state of higher repression potential; however, Southern analyses failed to reveal significant changes in the array of genomic P elements that could account for this evolution. In addition, none of the lines possessed the incomplete P element known as KP, which has been proposed to explain repression in some D. melanogaster strains. One of the lines maintained intermediate repression potential throughout the period of study (52 generations), indicating that the intermediate condition was not intrinsically unstable. Genetic analyses demonstrated that in some of the lines, repression potential was influenced by factors that were inherited maternally through at least two generations; however, these factors were not as influential as those in a classic P cytotype strain. Additional tests with a dysgenesis-inducing X chromosome called T-5 indicated that repression itself was mediated by a combination of maternal effects and paternally inherited factors that were expressed after fertilization. These tests also suggested that in some circumstances, the P transposase, or its message, might be transmitted through the maternal cytoplasm.


Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 1329C-1329C

Abstract In the paper by S. Ronsseray, M. Lehmann, D. Nouaud and D. Anxolabéhère (Genetics  143:  1663–1674; August, 1996) entitled “The regulatory properties of autonomous subtelomeric P elements are sensitive to a Suppresor of variegation in Drosophila melanogaster,” on page 1668 in the legend to Figure 2, line 4 should begin “representing the P element is oriented as follows: 5′◀3′.


1999 ◽  
Vol 21 (21) ◽  
pp. 51 ◽  
Author(s):  
Chirlei Cintia Klein ◽  
Liliana Essi ◽  
Ronaldo Medeiros Golombieski ◽  
Élgion Lúcio da Silva Loreto

Hybrid dysgenesis has been defined as a remarkable syndrome of correlated genetic traits that are produced in some particular crosses between certain strains. The present study main objective was classify recently collected Drosophila melanogaster strains in relation to P element activity and regulatory capacity. Our results to natural populations trapped from Rio Grande do Sul, Brazil and Colombia shows that it fell on Q class, since all examinated strains has showed P elements by molecular analysis and low P activity. In the same way, these strains shows low susceptibility to P element action. The bigger values found in the colombian population are in agreement with the clinal hypothesis to P element activity.


Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 205-215 ◽  
Author(s):  
Michael J Simmons ◽  
Kevin J Haley ◽  
Craig D Grimes ◽  
John D Raymond ◽  
Joseph C L Fong

Abstract Fusions between the Drosophila hsp70 promoter and three different incomplete P elements, KP, SP, and BP1, were inserted into the Drosophila genome by means of hobo transformation vectors and the resulting transgenic stocks were tested for repression of P-element transposase activity. Only the H(hsp/KP) transgenes repressed transposase activity, and the degree of repression was comparable to that of a naturally occurring KP element. The KP transgenes repressed transposase activity both with and without heat-shock treatments. Both the KP element and H(hsp/KP) transgenes repressed the transposase activity encoded by the modified P element in the P(ry+, Δ2-3)99B transgene more effectively than that encoded by the complete P element in the H(hsp/CP)2 transgene even though the P(ry+, Δ2-3)99B transgene was the stronger transposase source. Repression of both transposase sources appeared to be due to a zygotic effect of the KP element or transgene. There was no evidence for repression by a strictly maternal effect; nor was there any evidence for enhancement of KP repression by the joint maternal transmission of H(hsp/KP) and H(hsp/CP) transgenes. These results are consistent with the idea that KP-mediated repression of P-element activity involves a KP-repressor polypeptide that is not maternally transmitted and that KP-mediated repression is not strengthened by the 66-kD repressor produced by complete P elements through alternate splicing of their RNA.


Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 1857-1866 ◽  
Author(s):  
Stéphane Ronsseray ◽  
Laurent Marin ◽  
Monique Lehmann ◽  
Dominique Anxolabéhère

Abstract 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.


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