Polygenic Mutation

Mukai, Terumi

doi:10.1016/b978-0-12-688850-8.50016-7

Cited by 25 publications

(10 citation statements)

References 33 publications

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“…This argument is, of course, weakened if most new mutations are highly recessive, but it cannot be completely invalid unless mutant alleles are completely recessive. Neither of these conditions are compatible with the existing data (Mukai 1979). In any event, haploidy does not simply enhance the impact of mutations at the individual level by the elimination of masking.…”

Section: Discussionsupporting

confidence: 80%

“…Although data are available for only a small number of species (Bell 1988b;Charlesworth et al 1990;Crow and Simmons 1983;Houle et al 1992;Lynch and Gabriel 1990;Mukai 1979), it now seems clear that deleterious mutations arise at a high rate in most organisms. Summing over all loci, and to an order of magnitude, the deleterious mutation rate appears to be at least one per diploid genome per generation, and indirect evidence suggests it could be much higher (Kondrashov 1988).…”

mentioning

confidence: 99%

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The Mutational Meltdown in Asexual Populations

Lynch¹,

Bürger²,

Butcher³

et al. 1993

Journal of Heredity

575

499

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Loss of fitness due to the accumulation of deleterious mutations appears to be inevitable in small, obligately asexual populations, as these are incapable of reconstituting highly fit genotypes by recombination or back mutation. The cumulative buildup of such mutations is expected to lead to an eventual reduction in population size, and this facilitates the chance accumulation of future mutations. This synergistic interaction between population size reduction and mutation accumulation leads to an extinction process known as the mutational meltdown, and provides a powerful explanation for the rarity of obligate asexuality. We give an overview of the theory of the mutational meltdown, showing how the process depends on the demographic properties of a population, the properties of mutations, and the relationship between fitness and number of mutations incurred.

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Section: Discussionsupporting

confidence: 80%

mentioning

confidence: 99%

The Mutational Meltdown in Asexual Populations

Lynch¹,

Bürger²,

Butcher³

et al. 1993

Journal of Heredity

575

499

View full text Add to dashboard Cite

show abstract

“…If it is assumed that gene actions at the different loci and the effects of various environmental factors are independent and that there is no genotype-environment interaction, the following relationships hold: LI(R)N =ln A-lna [2] LI(R)Il =In B-ln b. [3] Thus, the difference between LI(R)N and LI(R)I(D) is measurable and expressed as follows: D=LI(R)N-LI(R)I = ln A-ln a-ln B +ln b [4] = ln (Ab/aB).…”

Section: Methodsmentioning

confidence: 99%

“…A chromosome carrying an inversion, In(2L)t, was introduced into the population about 1000 generations ago, as determined by the known rate of crossing over and the present frequency of a gene that has been introduced into the inversion by such crossovers. This is long enough for mildly deleterious and lethal mutations to reach equilibrium frequencies (2), and indeed the distribution of homozygous viabilities in the inverted chromosome is indistinguishable from that of the standard chromosomes. On the other hand, the time is not nearly long enough for polymorphic equilibria to be established (3), and this is confirmed by the near-monomorphism of three isozyme loci in or very near the inverted region.…”

mentioning

confidence: 99%

Selection of viability at loci controlling protein polymorphisms in Drosophila melanogaster is very weak at most.

Mukai¹,

Tachida²,

Ichinose³

1980

Proc. Natl. Acad. Sci. U.S.A.

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In an isolated Drosophila population the frequency of chromosomes carrying the second chromosome inversion In(2L)t is about 60%. Three isozyme loci are nearly monomorphic in the inversion-carrying chromosomes but are highly polymorphic in other chromosomes. From known recombination frequencies and the slight polymorphism, it is estimated that the inversion-carrying chromosomes are descended from one or a few identical chromosomes introduced about 1000 generations previously. This is long enough for lethal and mildly deleterious mutants to reach equilibrium frequencies but not long enough for very weakly selected mutants. Because the difference in viability between homozygous and heterozygous chromosomes is the same, it is inferred that there is at most very weak selection for isozyme loci. This method is sensitive enough to detect selective differences of 0.0005 per locus or less. One of the most important issues in population and evolutionary genetics is the mechanism whereby protein polymorphisms are maintained in populations. At present, most population geneticists agree in that, if selection is operating in the maintenance of protein polymorphisms, it must be quite weak (1). Because the experimental resolving power is limited, the minimal selection coefficient thus far estimated is of the order of 10-2 per locus (1). We have been able to increase the sensitivity to the order of 10-4.Drosophila melanogaster populations typically carry several cosmopolitan polymorphic inversions. These are supposed to have occurred uniquely some years ago and to have migrated to various places in the world. By utilizing the history of one type of inversion in one population, it may be possible to estimate the average selection intensity for very weakly selected polymorphic loci.Briefly, the argument is this. A chromosome carrying an inversion, In(2L)t, was introduced into the population about 1000 generations ago, as determined by the known rate of crossing over and the present frequency of a gene that has been introduced into the inversion by such crossovers. This is long enough for mildly deleterious and lethal mutations to reach equilibrium frequencies (2), and indeed the distribution of homozygous viabilities in the inverted chromosome is indistinguishable from that of the standard chromosomes. On the other hand, the time is not nearly long enough for polymorphic equilibria to be established (3), and this is confirmed by the near-monomorphism of three isozyme loci in or very near the inverted region. If such loci are maintained by strong heterotic selection there should be a substantial difference in viability between homozygotes and heterozygotes for the standard, equilibrium chromosomes but not within the nearly monomorphic chromosomes with the inversion. However, no such difference was found; the viability difference between homozygotes and heterozygotes was essentially the same in both groups, within about 1%. With an estimated 350 polymorphic loci and 20% heterozygotes (4, 5), this leads to the conclusion that...

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“…Such mutations appear to be approximately additive within loci (MUKAI 1979). If mutations on different loci act independently then the fitness reductions from each locus can be treated as multiplicative.…”

Section: Estimates For Mutation Rates and Selection Coeffiecientsmentioning

confidence: 99%

Population extinction by mutational load and demographic stochasticity

1993

Biological Conservation

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Polygenic Mutation

Cited by 25 publications

References 33 publications

The Mutational Meltdown in Asexual Populations

The Mutational Meltdown in Asexual Populations

Selection of viability at loci controlling protein polymorphisms in Drosophila melanogaster is very weak at most.

Population extinction by mutational load and demographic stochasticity

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