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W R Engels

Publications and source records attributed to W R Engels.

At least 37 records · Page 2Linked to original sources
PubMed1990

Germ-line and somatic recombination induced by in vitro modified P elements in Drosophila melanogaster.

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.

Animals↗
PubMed1989

Modified P elements that mimic the P cytotype in Drosophila melanogaster.

Activity of the P family of transposable elements in Drosophila melanogaster is regulated primarily by a cellular condition known as P cytotype. It has been hypothesized that P cytotype depends on a P element-encoded repressor of transposition and excision. We provide evidence in support of this idea by showing that two modified P elements, each with lesions affecting the fourth transposase exon, mimic most of the P cytotype effects. These elements were identified by means of two sensitive assays capable of detecting repression by a single P element. One assay makes use of cytotype-dependent gene expression of certain P element insertion mutations at the singed bristle locus. The other measures suppression of transposase activity from the unusually stable genomic P element, delta 2-3(99B), that normally produces transposase in both germinal and somatic tissues. The P cytotype-like effects include suppression of snw germline hypermutability, snw somatic mosaicism, pupal lethality, and gonadal dysgenic sterility. Unlike P cytotype, however, there was no reciprocal cross effect in the inheritance of repression.

Alleles↗
PubMed1988

P-M hybrid dysgenesis does not mobilize other transposable element families in D. melanogaster.

Mobilization of the P family of transposable elements in Drosophila melanogaster occurs in the hybrid progeny of males from an element-bearing strain (P strain) and females from an element-free strain (M strain). We tested whether the same crosses could mobilize other families of transposable elements. A mating scheme was used in which a set of X chromosomes was kept for 20 generations in either the active condition (known as hybrid dysgenesis) or the inactive condition (nondysgenic). Examination of 19 families of transposable elements by in situ hybridization indicated that only the P family was measurably mobilized under dysgenic conditions. Thus, P-M hybrid dysgenesis does not increase the transpositional activity of other families of transposable elements in D. melanogaster. We discuss possible explanations for several published reports to the contrary.

Animals↗
PubMed1988

A stable genomic source of P element transposase in Drosophila melanogaster.

A single P element insert in Drosophila melanogaster, called P[ry+ delta 2-3](99B), is described that caused mobilization of other elements at unusually high frequencies, yet is itself remarkably stable. Its transposase activity is higher than that of an entire P strain, but it rarely undergoes internal deletion, excision or transposition. This element was constructed by F. Laski, D. Rio and G. Rubin for other purposes, but we have found it to be useful for experiments involving P elements. We demonstrate that together with a chromosome bearing numerous nonautonomous elements it can be used for P element mutagenesis. It can also substitute efficiently for "helper" plasmids in P element mediated transformation, and can be used to move transformed elements around the genome.

Animals↗
PubMed1987

Somatic effects of P element activity in Drosophila melanogaster: pupal lethality.

Nonautonomous P elements normally excise and transpose only when a source of transposase is supplied, and only in the germline. The germline specificity depends on one of the introns of the transposase gene which is not spliced in somatic cells. To study the effects of somatic P activity, a modified P element (delta 2-3) lacking this intron was used as a source of transposase. Nonautonomous P elements from a strain called Birmingham, when mobilized in somatic cells by delta 2-3, were found to cause lethality, although neither component was lethal by itself. The three major Birmingham chromosomes acted approximately independently in producing the lethal effect. This lethality showed a strong dependence on temperature. Although temperature sensitivity was limited to larval stages, the actual deaths occurred at the pupal stage. Survivors, which could be recovered by decreasing the temperature or by reducing the proportion of the Birmingham genome present, often showed multiple developmental anomalies and reduced longevity reminiscent of the effects of cell death from radiation damage. Although the genetic damage occurred in dividing imaginal disc cells, the phenotypic manifestations--death and abnormalities--are not observed until later. The survivors also showed gonadal dysgenic (GD) sterility, a well-known characteristic of P-M hybrid dysgenesis. To explain these findings, we suggest that pupal lethality and GD sterility are both caused by massive chromosome breakage in larval cells, resulting from excision and transposition of genomic P elements acting as substrate for the transposase.

Animals↗
PubMed1986

On the evolution and population genetics of hybrid-dysgenesis-causing transposable elements in Drosophila.

Much has been learned about transposable genetic elements in Drosophila, but questions still remain, especially concerning their evolutionary significance. Three such questions are considered here. Has the behaviour of transposable elements been most influenced by natural selection at the level of the organism, the population, or the elements themselves? How did the elements originate in the genome of the species? Why are laboratory stocks different from natural populations with respect to their transposable element composition? No final answers to these questions are yet available, but by focusing on the two families of hybrid dysgenesis-causing elements, the P and I factors, we can draw some tentative conclusions.

Animals↗
PubMed1984

A trans-acting product needed for P factor transposition in Drosophila.

A transposable genetic element of the P family in Drosophila melanogaster was found to be unstable in the presence of other P elements but stable in their absence. A sensitive assay for P transpositional activity is provided by the snw allele, a defective P insert in the singed bristle locus which becomes hypermutable only in the presence of complete elements. This measure of activity was highly correlated with a type of female sterility normally associated with P activity. There was no cross-reactivity with transposase from another hybrid dysgenesis-causing element (the I factor).

Animals↗
PubMed1984

Formation of chromosome rearrangements by P factors in Drosophila.

We studied a collection of 746 chromosome rearrangements all induced by the activity of members of the P family of transposable elements in Drosophila melanogaster. The chromosomes ranged from simple inversions to complex rearrangements. The distribution of complex rearrangement classes was of the kind expected if each rearrangement came about from a single multibreak event followed by random rejoining of chromosome segments, as opposed to a series of two-break events. Most breakpoints occurred at or very near (within a few hundred nucleotide pairs) the sites of preexisting P elements, but these elements were often lost during the rearrangement event. There were also a few cases of apparent gain of P elements. In cases in which both breakpoints of an inversion retained P elements, that inversion was capable of reverting at high frequencies to the original sequence or something close to it. This reversion occurred with sufficient precision to restore the function of a gene, held-up-b, which had been mutated by the breakpoint. However, some of the reversions had acquired irregularities at the former breakpoints that were detectable either by standard cytology or by molecular methods. The revertants themselves retained the ability to undergo further rearrangements depending on the presence of P elements. We interpret these results to rule out the simplest hypotheses of rearrangement formation that involve cointegrate structures or homologous recombination. The data provide a general picture of the rearrangement process and its possible relationship to transposition.

Animals↗
PubMed1983

Evolution of altruistic behavior by kin selection: an alternative approach.

The evolution of altruistic and selfish behavior by kin selection has been analyzed previously by asking which types of behavior are favored by natural selection. A type of behavior is defined as a given cost/benefit ratio, c/b, in terms of Darwinian fitness. An alternative approach is to consider c/b itself as a quantitative character subject to natural selection and evolving toward an equilibrium. This approach allows consideration of a continuum of behavioral options as opposed to just two alternatives as in the previous work. Environmental restrictions on the availability of opportunities for fitness transactions are imposed so that the total benefit an individual can provide for or take from his relatives increases with his c/b ratio. General conditions for stable equilibria are derived. These depend only on the coefficient of relationship between donor and recipient (r) and the function describing the availability of benefit. They are independent of the heritability and variance in the population. Under weak selection, the equilibrium c/b ratio will be r/2 for altruistic behavior and 1/(2r) for selfish behavior. By contrast, standard theory predicts that all altruistic acts with c/b ratios less than r will be favored, and no equilibrium can be predicted except under certain special conditions where only two behavioral options are available. In general, these results show that evolution of the donor's behavior (altruism) tends to maximize the quantity rb--c, and evolution of the recipient (selfish behavior) maximizes b--rc.

Altruism↗
PubMed1981

Base substitutions, length differences and DNA strand asymmetries in the human G gamma and A gamma fetal globin gene region.

We have studied differences arising subsequent to the 5 kilobase pair (kb) duplication that led to the human G gamma and A gamma fetal globin genes. The local occurrence of base substitutions in the duplicated 5 kb region correlates positively with the local AT base pair content. This correlation also occurs in two mouse beta-globin genes and in two mouse immunoglobulin genes. The relationship is valid for transcribed or nontranscribed DNA and for DNA that contains only coding sequences. Length differences in the fetal globin duplicated regions correlate positively with the occurrence of short direct repeats of greater than or equal 5 base pairs. Path analysis of the interrelationships of base composition, base substitutions, repeats and length differences provides an integrated view of the relative effects on chromosomal changes of these variables and of selection. The distributions along the chromosome of simple sequences and of base compositions show highly significant local asymmetries between the transcribed and nontranscribed strands of the DNA, which permit us to divide the fetal globin gene region into chromosomal domains. Comparable domains are present in DNA from other sources, including the mammalian viruses SV40 and polyoma virus strain A-2 in which some of the domains appear related to discrete functions.

Animals↗
PubMed1981

Identifying P factors in Drosophila by means of chromosome breakage hotspots.

A syndrome of germline abnormalities in Drosophila melanogaster called hybrid dysgenesis is thought to be caused by transposable genetic elements known as P factors. Several lines of evidence presented here show that the chromosomal positions of at least some P factors can be identified as points of frequent chromosome breakage (hotspots). Starting with a strain (pi 2) in which four hotspots had been identified on the X chromosome, we found individual hotspots vanished when their part of the chromosome was replaced by the homologous part from a strain known to lack P factors. All hotspots in the non-substituted parts of the chromosome remained functional, indicating that they can act autonomously. We also observed a new breakage site coinciding with the appearance of an unstable mutation at the singed bristle locus (snW). This mutation was dysgenesis-induced, and previous genetic evidence suggested that it was caused by the insertion of a P factor at that locus. We also present preliminary evidence for rapid scrambling of the positions of hotspots under certain conditions, and we describe a new procedure for efficiently determining the positions of hotspots on a given chromosome.

Animals↗
PubMed1981

Estimating genetic divergence and genetic variability with restriction endonucleases.

Restriction endonucleases cut DNA at specific sites determined by the local nucleotide sequence. By comparing related DNA segments with respect to where such cuts are made, one can estimate the extent of sequence homology between the segments. Empirical methods are presented here for using these data to measure the proportion of mismatches between two sequences, the proportion of polymorphic positions in a series of sequences, or the degree of heterozygosity in a population. These methods do not require any assumptions concerning the evolutionary or population genetic processes involved. One can also use the data to calculate the precision of each of these estimates. When the positions of the cuts are not determined, these estimates can be made, using only the lengths of the resulting DNA fragments, by means of a maximum likelihood procedure. Several examples demonstrate the usefulness of these methods to study genetic differences in regions of the genome not amenable to study by other methods.

DNA↗
PubMed1980

Components of hybrid dysgenesis in a wild population of Drosophila melanogaster.

Hybrid dysgenesis is a condition found in certain interstrain hybrids of Drosophila melanogaster caused by the interaction of chromosomal and cytoplasmic factors. Germ-line abnormalities, including sterility, high mutability and male recombination, appear in the affected individuals. There are at lest two distinct systems of hybrid dysgenesis. We examined a Wisconsin wild population in two consecutive years to determine the distribution of the chromosomal P factor and the extrachromosomal M cytotype that together cause one kind of hybrid dysgenic sterility. The P factor was found to be very common in the population, with all three major chromosomes being polymorphic for it. This polymorphism was strongly correlated with variability for male recombination elements, suggesting that these two traits are part of the same system of hybrid dysgenesis. There was a slight tendency for the P factor to be lost in lines taken from this population and inbred in the laboratory for many generations. A large-scale search for the M cytotype, which causes susceptibility to the P factor, showed that it is present in the population at only very low frequencies. Further evidence that the population is mostly immune to the action of the P factor was our finding of a general lack of dysgenic sterility in the wild flies themselves. However, we were able to isolate several wild strains that consistently showed the M cytotype. In some cases, the frequency of the M cytotype could be maintained in these lines, but it could not usually be increased by artificial selection. Some possible consequences of hybrid dysgenesis for the evolutionary biology of Drosophila are suggested.

Animals↗