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R Frankham

Publications and source records attributed to R Frankham.

At least 19 recordsLinked to original sources
PubMed1997

Do island populations have less genetic variation than mainland populations?

Island populations are much more prone to extinction than mainland populations. The reasons for this remain controversial. If inbreeding and loss of genetic variation are involved, then genetic variation must be lower on average in island than mainland populations. Published data on levels of genetic variation for allozymes, nuclear DNA markers, mitochondrial DNA, inversions and quantitative characters in island and mainland populations were analysed. A large and highly significant majority of island populations have less allozyme genetic variation than their mainland counterparts (165 of 202 comparisons), the average reduction being 29 per cent. The magnitude of differences was related to dispersal ability. There were related differences for all the other measures. Island endemic species showed lower genetic variation than related mainland species in 34 of 38 cases. The proportionate reduction in genetic variation was significantly greater in island endemic than in nonendemic island populations in mammals and birds, but not in insects. Genetic factors cannot be discounted as a cause of higher extinction rates of island than mainland populations.

Animals↗
PubMed1996

Microsatellite polymorphisms in a wild population of Drosophila melanogaster.

Highly variable DNA polymorphisms called microsatellites are rapidly becoming the marker of choice in population genetic studies. Until now, microsatellites have not been utilized for Drosophila studies. We have identified eight polymorphic microsatellite loci in Drosophila melanogaster and used them to characterize the genetic variation in a wild population from the Tyrrell's winery in Australia. Microsatellites were isolated from a partial genomic DNA library. All microsatellites consist of (AC)n repeats ranging from n = 2 to n = 24. Six loci were assigned to chromosomal location by genetic mapping, with three loci on chromosome II, one locus on chromosome III and two loci on the X chromosome. Up to four microsatellite loci were multiplexed in the same reaction. Microsatellite variation is substantially greater than allozyme variation in the Tyrrell's Drosophila population. 80% of the microsatellite loci examined are polymorphic, compared with 28% of allozymes. The mean number of alleles per polymorphic locus is 5.2 in microsatellites compared with 3.0 in allozymes. The average observed heterozygosity of polymorphic microsatellites is 47% compared with 26% for allozymes. Microsatellite variation in Drosophila melanogaster is similar to that reported for other insects. Higher variability commends microsatellites over allozymes for genetic studies in Drosophila melanogaster.

Animals↗
PubMed1995

Conservation genetics.

Inbreeding depression, accumulation and loss of deleterious mutations, loss of genetic variation in small populations, genetic adaptation to captivity and its effect on reintroduction success, and outbreeding depression are reviewed. The impact of genetic factors in endangerment and extinction has been underestimated in some recent publications. Inbreeding depression in wildlife and in the field has been clearly established, while its impact has been greatly underestimated. The size of populations where genetic factors become important is higher than previously recognized, as Ne/N ratios average 0.11. Purging effects have been overestimated as a mechanism for eliminating deleterious alleles in small populations. The impact of loss of genetic variation in increasing the susceptibility of populations to environmental stochasticity and catastrophes has generally been ignored. Consequently, extinctions are often attributed to "nongenetic" factors when these may have interacted with genetic factors to cause extinction.

Adaptation, Biological↗
PubMed1994

Decline in heterozygosity under full-sib and double first-cousin inbreeding in Drosophila melanogaster.

The effects of inbreeding on heterozygosities and reproductive fitness were determined by carrying out full-sib and double first-cousin inbreeding in Drosophila melanogaster populations for up to 18 generations. Parents were scored each generation for five or six polymorphic enzyme loci, and progeny numbers per pair were recorded. Inbreeding depression, in the form of significant reductions in progeny numbers and significant extinction of lines, was observed. Heterozygosity decreased at a significantly slower rate than predicted, being about 80% of expected. The full-sib and double first-cousin treatments showed similar disagreement with expectations over comparable ranges of inbreeding. Natural selection was shown to favor heterozygotes in the inbred lines. Associative overdominance was the most probable explanation for the slower than expected decline in heterozygosity.

Alleles↗
PubMed1994

Modelling problems in conservation genetics using Drosophila: consequences of fluctuating population sizes.

Many natural populations fluctuate widely in population size. This is predicted to reduce effective population size, genetic variation, and reproductive fitness, and to increase inbreeding. The effects of fluctuating population size were examined in small populations of Drosophila melanogaster of the same average size, but maintained using either fluctuating (FPS) or equal (EPS) population sizes. FPS lines were maintained using seven pairs and one pair in alternate generations, and EPS lines with four pairs per generation. Ten replicates of each treatment were maintained. After eight generations, FPS had a higher inbreeding coefficient than EPS (0.60 vs. 0.38), a lower average allozyme heterozygosity (0.068 vs. 0.131), and a much lower relative fitness (0.03 vs. 0.25). Estimates of effective population sizes for FPS and EPS were 3.8 and 7.9 from pedigree inbreeding, and 4.9 vs. 7.1 from changes in average heterozygosities, as compared to theoretical expectations of 3.3 vs. 8.0. Results were generally in accordance with theoretical predictions. Management strategies for populations of rare and endangered species should aim to minimize population fluctuations over generations.

Animals↗
PubMed1994

Heat shock protein gene HSP108 and a replication histone gene cluster are linked in the chicken.

In work aimed at extending the chicken genome linkage map, a heat shock protein gene, HSP108, was shown by restriction fragment length polymorphism (RFLP) analysis to be linked to one of two replication histone gene clusters located on chromosome 1. Linkage was estimated using the LOD score method, on segregation data from seven pedigreed three-generation families (245 individuals). The maximum likelihood estimate of the recombination fraction (theta) was 0.215.

Animals↗
PubMed1992

Induced expression of a Drosophila hsp70 promoter-fusion transgene is reduced after repeated heat shocks.

Levels of transcripts produced by a heat shock protein 70 (hsp70)-antisense white transgene in Drosophila were measured after single and multiple heat shocks to determine whether the hsp70 promoter could produce sustained high levels of transgene transcripts. A single heat shock resulted in typical highly inducible levels of RNA, but the amount of antisense RNA was substantially reduced after multiple heat shocks. Endogenous hsp70 mRNA levels were also less abundant after multiple heat shocks as compared to a single heat shock. The hsp70 promoter is unsuitable for use in fusion gene constructs for long term expression studies where repeated heat shocks are required.

Animals↗
PubMed1991

Heterozygosity at protein loci in inbred and outbred lines of chickens.

Levels of heterozygosity at six polymorphic protein marker loci were determined by electrophoresis in 24 lines of poultry, encompassing 17 White Leghorn inbred lines (WLI) (with inbreeding coefficients, F, ranging from .946 to .988), five Australorp inbred lines (AusI) (with F values ranging from .924 to .961), and two randombred lines (one White Leghorn and one Australorp). Fixation was observed at one locus in WLI lines, and at two loci in the AusI lines. Segregation at the other loci was observed in the inbred lines of the two breeds. Observed heterozygosity in the inbred lines markedly exceeded the expectations under inbreeding theory. In White Leghorns, reproductive fitnesses for heterozygotes were superior to homozygotes in the inbred lines, but not in the control. Consequently, natural selection operating through associative overdominance appears to be responsible for the higher than expected heterozygosities in the inbred lines.

Animals↗
PubMed1990

Adding the heterochromatic YL arm to an X chromosome reduces reproductive fitnesses in Drosophila melanogaster: implications for the evolution of rDNA, heterochromatin, and reproductive isolation.

For X-Y exchange to be of importance in the coevolution of X and Y rDNA, there must be a mechanism to maintain cytologically normal X chromosomes in the face of continual infusions of X.YL chromosomes produced by X-Y exchanges. Replicated populations were founded with different frequencies of isogenic X and X.YL chromosomes. The X.YL chromosome declined in frequency over time in all lines. Relative fitnesses, estimated from chromosome frequency trajectories, were 0.40, 1.01, and 1.0 for X.YL/X.YL, X.YL/X, and X/X females and 0.75 and 1.0 for X.YL/Y and X/Y males, respectively. The equilibrium frequency for the X.YL chromosome due to the balance between X-Y exchange and selection was predicted to be 4-16 x 10(-4). The results strengthen the evidence for the involvement of X-Y exchange in the coevolution of X and Y rDNA arrays. Conditions for the evolution of reproductive isolation by sex-chromosome translocation are much less probable than previously supposed since the X.YL translocation chromosome is at a selective disadvantage to cytologically normal X chromosomes. Additional heterochromatin was not neutral but was only deleterious beyond a threshold, as one dose of the heterochromatic XL arm did not reduce female reproductive fitness, but two doses did.

Animals↗
PubMed1988

Molecular hypotheses for position-effect variegation: anti-sense transcription and promoter occlusion.

There is currently no comprehensive molecular hypothesis to account for position-effect variegation, the mosaic expression of a gene lying near a breakpoint of a chromosomal rearrangement. Here it is proposed that position-effect variegation arises from either anti-sense transcription or from promoter occlusion (transcription readthrough), the former mechanism operating for breakpoints on the 3' side of the affected gene and the latter for breakpoints on the 5' side. Anti-sense transcription will occur in rearrangements that place the anti-sense strand of genes next to a promoter. This anti-sense RNA hybridizes to, and thereby inactivates, sense mRNA transcripts (as anti-sense RNA is known to do). Promoter occlusion may occur in rearrangements that place the affected gene near an open upstream promoter. This promoter drives readthrough transcription that inhibits most normal transcripts. Occasional normal transcripts lead to phenotypic variegation. These hypotheses have three strengths: (i) they predict the major observed features of position-effect variegation including variegated phenotype, stable inheritance, the involvement of rearrangements, only some rearrangements causing variegation, the occurrence of both dominant and recessive variegation, the spreading effect of variegation to several loci, and the conditions required for expression of variegation; (ii) they can plausibly account for features of position-effect variegation that they do not specifically predict; (iii) they lead to a series of novel and testable predictions, including the presence of altered transcripts in rearrangements including position-effect variegation, the location of breakpoints required to cause variegation, and a correlation between the extent of the spreading effect and the length of the novel transcript. These mechanisms can account for several other cases of variegation in addition to classic position-effect variegation. Actual or putative examples of phenotypic variegation due to these mechanisms are known.

Animals↗
PubMed1980

Unequal crossing over at the rRNA tandon as a source of quantitative genetic variation in Drosophila.

Abdominal bristle selection lines (three high and three low) and controls were founded from a marked homozygous line to measure the contribution of sex-linked "mutations" to selection response. Two of the low lines exhibited a period of rapid response to selection in females, but not in males. There were corresponding changes in female variance, in heritabilities in females, in the sex ratio (a deficiency of females) and in fitness, as well as the appearance of a mutant phenotype in females of one line. All of these changes were due to bb alleles (partial deficiencies for the rRNA tandon) in the X chromosomes of these lines, while the Y chromosomes remained wild-type bb+. We argue that the bb alleles arose by unequal crossing over in the rRNA tandon.--A prediction of this hypothesis is that further changes can occur in the rRNA randon as selection is continued. This has now been shown to occur.--Our minimum estimate of the rate of occurrence of changes at the rRNA tandom is 3 X 10(-4). As this is substantially higher than conventional mutation rates, the questions of the mechanisms and rates of origin of new quantitative gaenetic variation require careful re-examination.

Animals↗
PubMed1977

The nature of quantitative genetic variation in Drosophila. III. Mechanism of dosage compensation for sex-linked abdominal bristle polygenes.

Seventeen lines, each homozygous for a different X chromosome but all with a common autosomal genetic blackground, were constructed and assayed for abdominal bristle number to determine whether dosage compensation operates for sex-linked genes affecting this character. --The regression coefficient of male mean on female mean using a logarithmic scale was 0.90 +/- 0.13 and the genetic regression coefficient 0.92, neither differing significantly from unity. The genetic components of variance in males and females were also very similar (0.000234 or 0.000228, respectively). These results indicate that dosage compensation is complete (or nearly so) for sex-linked genes affecting this character. The bristle scores of females did not differ in reciprocal crosses between these lines, thus dosage compensation does not operate by paternal X inactivation. --The question of an adequate scale for abdominal bristle number had to be examined during the study. A logarithmic scale appeared to be adequate for both genotypic and environmental differences.

Animals↗