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J A Sved

Publications and source records attributed to J A Sved.

18 recordsLinked to original sources
PubMed1991

High levels of recombination induced by homologous P elements in Drosophila melanogaster.

P element transposons in Drosophila melanogaster are capable of mobilizing incomplete P elements elsewhere in the genome, and of inducing recombination. This recombination is usually only of the order of 1% or less. We show that two P elements, located at exactly homologous sites, induce levels of recombination of 20% or higher. The recombination appears to be exact, as determined by the lack of phenotypic effects in recombinant products and the lack of size changes detectable by Southern hybridization. Female recombination is increased, but to a lesser extent than male recombination. Somatic recombination levels are also elevated. Alternative explanations for the high recombination levels are given in terms of the consequences of repair of an excision site and in terms of recombination as part of the replicative transposition process.

Animals↗
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↗
PubMed1990

Population genetic consequences of the fragile-X syndrome, based on the X-inactivation imprinting model.

We have examined the population genetic consequences of the model of Laird (Genetics 117:587-599, 1987) in which the fragile-X syndrome is caused by "imprinting" of a mutant chromosome. The imprinting event in this model results from a block to reactivation of an inactive X chromosome prior to oogenesis. If it is assumed that males carrying the imprinted chromosome never reproduce, the frequencies of females and males carrying the imprinted chromosome are expected to be equal. When a mutation-selection balance is established, there are expected to be somewhat more than twice as many females carrying the nonimprinted fragile X as carry the imprinted fragile-X chromosome, the excess depending on the fertility of fragile-X females. Nonpenetrant (transmitting) males, i.e., those with the nonimprinted fragile-X chromosome, are expected to be present at about the same frequency as are males with the syndrome. More than one-third of the nonimprinted chromosomes in the population are expected to be newly arisen in each generation. We have considered possible alternatives to the model of a mutation-selection balance. Nonimprinted carrier females would need to have 100% fertility excess to avoid postulating a high mutation rate to account for the very high prevalence of the syndrome.

Dosage Compensation, Genetic↗
PubMed1987

Hybrid dysgenesis in Drosophila melanogaster: evidence from sterility and southern hybridization tests that P cytotype is not maintained in the absence of chromosomal P factors.

A two-generation crossing program was used to replace the entire chromosome complement of P strains by M strain chromosomes, the maternal contribution being from the P strain. The cytotype of chromosomally substituted females was indistinguishable from M strain cytotype, judged by the sterility of offspring from the cross of such females to P strain males. In addition, following replacement of the chromosomes, the level of DNA homologous to the P factor was sufficiently low to be explicable by low levels of P factor transposition. These results are consistent with immediate chromosomal control for the switching from P to M cytotype. However, the reverse chromosome substitution, replacing all chromosomes of an M strain with P chromosomes, did not usually lead to immediate change of cytotype properties, showing that there is a true maternal effect in the M to P direction. The absence of true maternal inheritance for P cytotype argues against models of P factor repression which depend on autonomous replication of a nonchromosomal element. The repression could still be explained by nonchromosomal copies of the P factor, provided that these are replenished from chromosomal P factors. A model is put forward in which P cytotype is due to the presence of circular P factors carrying a P factor target sequence, leading to preferential transposition of chromosomal P factors to nonchromosomal target sites.

Animals↗
PubMed1980

Similarity of centromeric heterochromatin in strains of drosophila melanogaster which interact to produce hybrid dysgenesis.

Many long-established laboratory strains of D. melanogaster interact with recently-collected wild-type strains, so that the progeny show sterility, enhanced mutation, male recombination and other degenerative traits, a syndrome known collectively as "hybrid dysgenesis". Tests have been made for differences in centromeric heterochromatin between interacting strains, by comparing homologues in mitotic preparations from hybrid individuals. Differences between homologues have not been revealed, either qualitatively by C-banding or quantitatively by in situ hybridisation to RNA transcripts from satellites 1.705 and 1.686. However, the sensitivities of the techniques are such that quantitative differences of less than 50% between strains could escape detection.

Animals↗
PubMed1977

Migration and mutation in stochastic models of gene frequency change. I. The island model.

Migration has in the past been introduced deterministically into stochastic gene frequency models. Migration at rate m then reduces the between-population variability by a factor of (1 - m)2 each generation. We show that with stochastic migration, whether of fixed or variable numbers of individuals, a positive term delta m is added to the variance. As a result of the delta m term, the equilibrium value of the between-population variability is increased compared to the corresponding value for deterministic migration by a factor of approximately (1 - m)-2 for small m. An equivalent result is derived for mutation, using the infinite allele model for a single population. We show in addition that these results may be derived much more simply by use of identity-by-descent probability methods, but only if a modified definition of the probability of identity-by-descent is used, involving the sampling with instead of without replacement of pairs of genes from the population.

Diploidy↗
PubMed1976

Hybrid dysgenesis in Drosophila melanogaster: a possible explanation in terms of spatial organization of chromosomes.

Male recombination and female sterility, two aspects of hybrid dysgenesis in D. melanogaster, have been studied in crosses between a locally collected wild population and laboratory strains. Dysgenesis occurs in the F1 hybrid of such crosses only if the wild type is used as male parent and the laboratory strain as female, suggesting an interaction between genotype and cytoplasm. However the results from further crosses are difficult to interpret in terms of a conventional genotype-cytoplasm model, and suggest that for dysgenesis to occur it is necessary that the wild-type chromosomes be contributed by the male parent. Furthermore, receipt of any of the three major wild-type chromosomes in crosses to laboratory females is sufficient to cause hybrid dysgenesis. A model in terms of spatial organization of chromosomes is put forward to explain these results. It is postulated that (1) normal nuclear functioning requires a definite spatial organization of chromosomes, which is presumably achieved by chromosome-membrane associations, (2) chromosomes are inherited from the female parent with spatial ordering preserved, i.e. membranes and associated chromosomes are handed on directly from the female parent, (3) spatial ordering is not necessarily preserved in male gametes, and paternally derived chromosomes carry information enabling them to become correctly organized within the zygote nucleus, and (4) hybrid dysgenesis results when the chromosome(s) from the male of one strain lack the information to become correctly organized in the nucleus of a second strain. The model seems to explain all aspects of the results, and offers the possibility that the present system may yield information on the genetics of membrane development and other aspects of spatial organization in the normal nucleus.

Animals↗