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Biomedical subjects

J A Sved

Publications and source records attributed to J A Sved.

At least 19 recordsLinked to original sources
PubMed2003

Inferring modes of colonization for pest species using heterozygosity comparisons and a shared-allele test.

Long-range dispersal of a species may involve either a single long-distance movement from a core population or spreading via unobserved intermediate populations. Where the new populations originate as small propagules, genetic drift may be extreme and gene frequency or assignment methods may not prove useful in determining the relation between the core population and outbreak samples. We describe computationally simple resampling methods for use in this situation to distinguish between the different modes of dispersal. First, estimates of heterozygosity can be used to test for direct sampling from the core population and to estimate the effective size of intermediate populations. Second, a test of sharing of alleles, particularly rare alleles, can show whether outbreaks are related to each other rather than arriving as independent samples from the core population. The shared-allele statistic also serves as a genetic distance measure that is appropriate for small samples. These methods were applied to data on a fruit fly pest species, Bactrocera tryoni, which is quarantined from some horticultural areas in Australia. We concluded that the outbreaks in the quarantine zone came from a heterogeneous set of genetically differentiated populations, possibly ones that overwinter in the vicinity of the quarantine zone.

Animals↗
PubMed2001

Microsatellite analysis of the Queensland fruit fly Bactrocera tryoni (Diptera: Tephritidae) indicates spatial structuring: implications for population control.

The population structure of a tephritid pest species, the Queensland fruit fly Bactrocera tryoni (Froggatt), has been analysed over a five year period (1994-1998), using six microsatellites. Adult fly samples were collected to cover most regions of eastern and central Australia where the flies are regularly found. Tests for heterogeneity indicated that flies within geographically defined regions were homogeneous. The samples were allocated into five regions, including one very large region, Queensland, which encompasses that portion of the fly's range where breeding can occur year-round. With one exception, the collections from different regions were homogeneous between years, showing a fairly static distribution of the species. However, differences between regions were highly significant. The one case of a change in frequency between years indicated a gradual replacement of flies in a marginal region by flies from the main part of the range. The finding of stability in the distribution of a highly mobile insect is of interest, potentially also for other species which have expanded beyond their native range. It is argued that a contributing reason for this stability may be adaptation to different climatic regimes, and that strategies for control based on this hypothesis afford a reasonable chance of success.

Animals↗
PubMed1998

Structure and associated mutational effects of the cysteine proteinase (CP1) gene of Drosophila melanogaster.

The complete structure of the cysteine proteinase (CP1) gene reveals two large 5' introns as well as a small third intron. Deletion studies have shown that null mutations for the locus are female sterile with partial male sterility as well as wing and pigmentation effects. Null alleles can be produced by either deletions to the left or deletions to the right of a P element insertion in the long second intron of the gene. A nearby phenylalanyl tRNA synthetase gene (Pts) was also identified.

Animals↗
PubMed1998

Polymorphic microsatellite markers for population analysis of a tephritid pest species, Bactrocera tryoni.

To obtain a set of microsatellite markers for the Queensland fruit fly Bactrocera tryoni, a genomic library was screened with a number of simple repeat oligonucleotide probes. Sequencing recovered 22 repeat loci. The microsatellite sequences were short, with repeat numbers ranging from five to 11. Of these, 16 polymerase chain reaction (PCR) primer sets yielded amplifiable products, which were tested on 53 flies from five widely separated sites. All loci showed polymorphism in the population sample, with the number of alleles ranging from two to 16. Several dinucleotide repeats showed alleles separated by single-base differences and multiple steps, suggesting a mutation process more complex than the stepwise mutation model.

Alleles↗
PubMed1998

Mitotic and polytene chromosome analyses in the Queensland fruit fly, Bactrocera tryoni (Diptera: Tephritidae).

The Queensland fruit fly, Bactrocera tryoni, like the Mediterranean fruit fly, Ceratitis capitata, has a diploid complement of 12 chromosomes, including five pairs of autosomes and a XX/XY sex chromosome pair. Characteristic features of each chromosome are described. Chromosomal homology between B. tryoni and C. capitata has been determined by comparing chromosome banding pattern and in situ hybridisation of cloned genes to polytene chromosomes. Although the evidence indicates that a number of chromosomal inversions have occurred since the separation of the two species, synteny of the chromosomes appears to have been maintained.

Animals↗
PubMed1997

The accumulation of P-element-induced recombinants in the germline of male Drosophila melanogaster.

P-element-induced recombination in Drosophila melanogaster occurs premeiotically. Recombinants are therefore expected to accumulate in the stem cells of the germline of P-element-carrying males. We show that both the recombination frequency and the incidence of "clustering" increase with the age of males carrying various P-element derivatives. The combination of end-deleted elements can lead to average recombination frequencies >50% with individual instances of 100% recombination. These elements also lowered the fertility of the carriers. We investigated these features by constructing an analytical and a computer simulation model of the course of events in the germline, incorporating the recently proposed hybrid element insertion (HEI) model of P-element activity. The model is able to predict extreme recombination levels, segregation ratio biases and lowered fertility through cell death in a single analysis.

Animals↗
PubMed1996

P-element-induced recombination in Drosophila melanogaster: hybrid element insertion.

It has previously been shown that the combination of two deleted P elements in trans, one containing the left functional end and the second element the right functional end, can lead to high levels of male recombination. This finding strongly suggests that P-element ends from different chromosomes can become associated, followed by "pseudo-excision". We show that two different processes are involved in resolving the pseudo-excision event: (1) the excised P-element ends continue to function as a single unit (Hybrid Element) and insert at a nearby site in the chromosome or into the element itself [Hybrid Element Insertion (HEI)] and (2) free ends that do not contain P elements repair and rejoin [(Hybrid Excision and Repair (HER)]. Both types of resolution can lead to recombination, and this paper concentrates on the HEI class. One type of HEI event predicts the exact reverse complementary duplication of an 8-bp target site, and we have confirmed the existence of such a structure in six independently derived recombinant chromosomes. There is also a high tendency for insertion events to occur within a few bases of the original 8-bp target site, including six apparent cases of insertion into the exact site.

Animals↗
PubMed1996

Flanking duplications and deletions associated with P-induced male recombination in Drosophila.

We studied P element-induced recombination in germline mitotic cells by examining the structure of the recombinant chromosomes. We found that most recombinants retain a mobile P element at the site of the recombination, usually with either a deletion or a duplication immediately adjacent to the P end at which the crossover occurred. The sizes of these deletions and duplications ranged from a few base pairs to well over 100 kb. These structures fit the "hybrid element insertion" (HEI) model of male recombination in which the two P-element copies on sister chromatids combine to form a "hybrid element" whose termini insert into a nearby position on the homologue. The data suggest that P-induced recombination can be used as an efficient means of generating flanking deletions in the vicinity of existing P elements. These deletions are easily screened using distant flanking markers, and they can be chosen to extend in a given direction depending on which reciprocal recombinant type is selected. Furthermore, the retention of a mobile P element allows one to extend the deletion or generate additional variability at the site by subsequent rounds of recombination.

Animals↗
PubMed1995

Male recombination with single and homologous P elements in Drosophila melanogaster.

It has previously been shown that, in the presence of a source of P element transposase, male recombination in Drosophila melanogaster is induced at a rate of about 1% in the region of a single P[CaSpeR] element. This paper shows that recombinant chromosomes retain unaltered P[CaSpeR] elements at the original site in a high proportion of cases. This result is incompatible with a simple model in which recombination occurs by resolution of a Holliday junction following P element excision and repair. It has also previously been shown that homozygous regions containing a P element produce male recombination levels of 10-20%, an order of magnitude higher than that given by a single element. This paper shows that reciprocal recombinant chromosomes retaining P[CaSpeR] elements can be combined to produce similarly high levels of recombination. This result potentially allows for recombinant chromosomes from homologous recombination to be analysed at the molecular level in the region of the inserted element.

Animals↗
PubMed1995

P-element-induced male recombination can be produced in Drosophila melanogaster by combining end-deficient elements in trans.

Male recombination, not normally present in Drosophila melanogaster, can be produced at high rates when target P elements at homologous sites are combined in the presence of transposase protein. We have produced a set of elements by in situ deletion of a particular insertion and have found elements that have deletions stretching into either end. Elements were tested in pairs to see whether they complement each other in their ability to induce recombination. The combination of elements that are deficient for the same end produces very little recombination, but the combination of a right-end and a left-end element can generate recombination values higher than given by two complete P[CaSpeR] elements at homologous sites. This strongly suggests that "hybrid" P elements, containing ends from two different elements, can be recognized by transposase protein. We have also examined genotypes containing a normal and an end-deficient element and found that they yield reasonably high levels of recombination. We interpret the resultant gametes from such genotypes as showing that the majority of events in this genotype derive from the association of complementary ends from the same element, whereas the complementary ends from elements in trans associate in only a minority of cases.

Animals↗
PubMed1994

A reevaluation of data from competitive tests shows high levels of heterosis in Drosophila melanogaster.

We have analyzed the results from a range of procedures designed to measure the fitness under competitive conditions of inbred strains of Drosophila melanogaster, specifically strains which are homozygous for chromosome 2. All methods show a substantial reduction in fitness, ranging from an estimated 70-80% for single generation competition tests to 80-90% for a multiple generation population cage procedure. Furthermore, inbreeding through brother-sister mating reduces fitness by a comparable amount when allowance is made for the expected degree of homozygosity.

Animals↗
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↗