Balancer Chromosome

Keyword(s):  

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1991-2001 ◽  
Author(s):  
A García-Dorado ◽  
A Caballero

Abstract T. Mukai and co-workers in the late 1960s and O. Ohnishi in the 1970s carried out a series of experiments to obtain direct estimates of the average coefficient of dominance (h¯) of minor viability mutations in Drosophila melanogaster. The results of these experiments, although inconsistent, have been interpreted as indicating slight recessivity of deleterious mutations, with h¯≈0.4. Mukai obtained conflicting results depending on the type of heterozygotes used, some estimates suggesting overdominance and others partial dominance. Ohnishi's estimates, based on the ratio of heterozygous to homozygous viability declines, were more consistent, pointing to the above value. However, we have reanalyzed Ohnishi's data, estimating h¯ by the regression method, and obtained a much smaller estimate of ~0.1. This significant difference can be due partly to the different weighting implicit in the estimates, but we suggest that this is not the only explanation. We propose as a plausible hypothesis that a putative nonmutational decline in viability occurring in the first half of Ohnishi's experiment (affecting both homozygotes and heterozygotes) has biased upward the estimates from the ratio, while it would not bias the regression estimates. This hypothesis also explains the very high h¯≈0.7 observed in Ohnishi's high-viability chromosomes. By constructing a model of spontaneous mutations using parameters in the literature, we investigate the above possibility. The results indicate that a model of few mutations with moderately large effects and h¯≈0.2 is able to explain the observed estimates and the distributions of homozygous and heterozygous viabilities. Accounting for an expression of mutations in genotypes with the balancer chromosome Cy does not alter the conclusions qualitatively.



Genetics ◽  
1996 ◽  
Vol 144 (4) ◽  
pp. 1993-1999 ◽  
Author(s):  
Peter D Keightley

Much population genetics and evolution theory depends on knowledge of genomic mutation rates and distributions of mutation effects for fitness, but most information comes from a few mutation accumulation experiments in Drosophila in which replicated chromosomes are sheltered from natural selection by a balancer chromosome. I show here that data from these experiments imply the existence of a large class of minor viability mutations with approximately equivalent effects. However, analysis of the distribution of viabilities of chromosomes exposed to EMS mutagenesis reveals a qualitatively different distribution of effects lacking such a minor effects class. A possible explanation for this difference is that transposable element insertions, a common class of spontaneous mutation event in Drosophila, frequently generate minor viability effects. This explanation would imply that current estimates of deleterious mutation rates are not generally applicable in evolutionary models, as transposition rates vary widely. Alternatively, much of the apparent decline in viability under spontaneous mutation accumulation could have been nonmutational, perhaps due to selective improvement of balancer chromosomes. This explanation accords well with the data and implies a spontaneous mutation rate for viability two orders of magnitude lower than previously assumed, with most mutation load attributable to major effects.



2008 ◽  
Vol 90 (3) ◽  
pp. 253-258 ◽  
Author(s):  
ERIC W. CROSS ◽  
MICHAEL J. SIMMONS

SummaryMutations in the RNA interference (RNAi) genes aubergine (aub), homeless and piwi were tested for effects on the frequency, distribution and coincidence of meiotic crossovers in the long arm of the X chromosome. Some increases in crossover frequency were seen in these tests, but they may have been due to a maternal effect of the balancer chromosomes that were used to maintain the RNAi mutations in stocks rather than to the RNAi mutations themselves. These same balancers produced strong zygotic interchromosomal effects when tested separately. Mutations in aub and piwi did not affect the frequency of crossing over in the centric heterochromatin of chromosome II; nor did a balancer chromosome III.



1979 ◽  
Vol 34 (3) ◽  
pp. 303-315 ◽  
Author(s):  
A. N. Wilton ◽  
J. A. Sved

SUMMARYPopulation cages were set up containing an X-chromosome balancer, and either a single wild-type chromosome(homozygous cages) or a mixture of wild-type chromosomes(heterozygous cages). The balancer chromosome was eliminated more rapidly from the heterozygous cages, indicating that chromosome heterozygotes are at an advantage over chromosome homozygotes. The disadvantage of X-chromosome homozygosity in the female is estimated to be about 40%. From earlier studies it is known that the average disadvantage of homozygosity for either of the two major autosomes of D. melanogaster is approximately 80%. Since these autosomes are both about twice as long as the X chromosome, the disadvantage per unit length is similar for both chromosomal types.Both X-chromosomal and autosomal heterosis can be explained by either dominance or overdominance at individual loci. However, a dominance model can only explain the similarity if many of the X-linked loci (about 50%) are limited in expression to the female.



1989 ◽  
Vol 53 (2) ◽  
pp. 129-140 ◽  
Author(s):  
Alan N. Wilton ◽  
Michael G. Joseph ◽  
John A. Sved

SummaryHigh levels of chromosomal heterosis have previously been detected in Drosophila using the balancer chromosome equilibration (BE) technique, in which single wild-type chromosomes are introduced into population cages along with a dominant/lethal balancer chromosome. The balancer chromosome is rarely eliminated in such populations, showing that the fitness of chromosome homozygotes must be low by comparison with chromosomal heterozygotes. As with all cases of chromosomal heterosis, the underlying cause could either be deleterious recessives at various loci or generalized overdominance. The experiment of the present paper examines the first of these explanations. Population cages containing just two wild-type chromosomes (dichromosomal populations) were set up and allowed to run for many generations. Single chromosomes were then re-extracted from these populations, and their fitness measured using the BE technique. Our expectation was that the gradual elimination of recessive genes from the dichromosomal populations ought to result in an increase in the fitness of such re-extracted chromosome homozygotes. Yet in two replicated experiments we were unable to demonstrate an; unequivocal increase in fitness. We have estimated the rate of increase of fitness under multiple locus dominance and partial dominance models. The principal unknown parameter in these calculations is the selection intensity per locus, s. The expected increase is approximately proportional to s, and we estimate that values of s around 1/64 should be detectable in our experiments. However linkage is expected to reduce the efficiency of the dichromosomal procedure We show by computer simulation that this reduction is by a factor of approximately 2, thus increasing the detectable level of s to approximately 1/32. Consideration of mutation-selection balance models shows that this is a feasible selection intensity only if dominance is nearly complete. Thus we are unable to rule out the notion that the genes responsible for heterosis are maintained by a simple mutation-selection balance, but the experimental results constrain the parameters of such a model to a narrow range.



Genetics ◽  
1976 ◽  
Vol 84 (2) ◽  
pp. 287-310
Author(s):  
Theodore R F Wright ◽  
Glenn C Bewley ◽  
Allen F Sherald

ABSTRACT Of 84 lethals isolated over the dopa decarboxylase (DDC) deficiency Df(2L)50, 8 have been identified as DDC-deficient alleles on the basis of their effect on DDC activity when heterozygous over the CyO balancer chromosome with activities ranging from 28% to 53% of controls. Some of the Ddc-deficient alleles exhibit intracistronic complementation. Most of the complementing pairs of alleles are much reduced in viability, e.g. < 5% of expected, and express a common syndrome of mutant phenes which can reasonably be inferred to derive from inadequately sclerotinized cuticle. Individuals heterozygous for the noncomplementing allele, Ddcn7, over the 12-band DDC deficiency, Df(2L)130, die at the end of embryogenesis as unhatched larvae with unpigmented mouth parts. The Ddc alleles and the l(2)amd α-methyl dopa (αMD) hypersensitive alleles are both located within the 11 band region 37B10-C7. The l(2)amd locus is immediately to the right of hk(2-53.9).Ddc has been mapped within 0.004 Map Units to the right of l(2)amd with a maximum estimated recombination frequency of 0.01%. None of the Ddc/CyO strains are sensitive to the dietary administration of α-methyl dopa (αMD), and complementation occurs between the Ddc deficient alleles and the l(2)amd alleles both on the basis of viability and DDC activity. No effect on DDC by the amd alleles has been found to date. Even in the complementing heterozygote, amdH1/amdH89, the level of activity, thermostability, and in vitro αMD inhibition of DDC remains unaffected. Although no biochemical phene has yet been established for the αMD hypersensitive amd alleles, it seems likely that the two groups of mutants are functionally related.



Genetics ◽  
1984 ◽  
Vol 106 (1) ◽  
pp. 95-107
Author(s):  
Walter F Eanes

ABSTRACT Several biochemical studies have suggested that in Drosophila melanogaster the two common allozymes of G6PD differ in their in vitro activities and thermal stabilities. Yet, it remains to be shown that these characterizations reflect actual in vivo differences and are not artifacts of the biochemical approach. In this study it is shown that in vivo activity differences must exist between these two variants. This conclusion arises from the observation that the viability of flies bearing a low activity allele of 6PGD is strongly dependent on the genotype at the G6PD (Zw) locus, whereas no measurable difference in viability can be detected between Zw genotypes in a normal activity 6PGD background. These viability interactions are in the direction predicted by the reported in vitro activities of the allozymes and the proposed deleterious effects of 6-phosphogluconate accumulation.—In addition, a genetic scheme is used that uncouples and quantifies the effects of viability modifiers in the region of the Zw locus, while homogenizing 98% of the X chromosome. The viability of different Zw genotypes is measured by examining whole chromosome viabilities relative to the FM6 balancer chromosome. The advantages of this particular scheme are discussed.



Genetics ◽  
1985 ◽  
Vol 111 (4) ◽  
pp. 831-844
Author(s):  
Walter F Eanes ◽  
Jody Hey ◽  
David Houle

ABSTRACT We report here a study of viability inbreeding depression associated with the X chromosome of Drosophila melanogaster. Fifty wild chromosomes from Mt. Sinai, New York, and 90 wild chromosomes from Death Valley, California, were extracted using the marked FM6 balancer chromosome and viabilities measured for homozygous and heterozygous females, and for hemizygous males, relative to FM6 males as a standard genotype. No statistically significant female genetic load was observed for either chromosome set, although a 95% confidence limit estimated the total load <0.046 for the samples pooled. About 10% of the Death Valley chromosomes appear to be "supervital" as homozygotes. There is little evidence for a pervasive sex-limited detrimental load on the X chromosome; the evidence indicates nearly identical viability effects in males and homozygous females excluding the supervital chromosomes. The average degree of dominance for viability polygenes is estimated between 0.23 to 0.36, which is consistent with autosomal variation and implies near additivity. We conclude that there is little genetic load associated with viability variation on the X chromosome and that the substantial reduction in total fitness observed for chromosome homozygosity in an earlier study may be due largely to sex-limited fertility in females.



2006 ◽  
Vol 6 (6) ◽  
pp. 653-665 ◽  
Author(s):  
Kathryn E. Hentges ◽  
Hisashi Nakamura ◽  
Yasuhide Furuta ◽  
Yuejin Yu ◽  
Debrah M. Thompson ◽  
...  


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