scholarly journals Fixation of New Mutations in Small Populations

2004 ◽  
pp. 155-170 ◽  
Author(s):  
Michael C. Whitlock ◽  
Reinhard Bürger
Keyword(s):  
Small Populations ◽  
New Mutations

scholarly journals Effects of linkage on response to directional selection from new mutations

1983 ◽  
Vol 42 (2) ◽  
pp. 193-206 ◽  
Author(s):  
P. D. Keightley ◽  
W. G. Hill
Keyword(s):  
Quantitative Traits ◽  
Directional Selection ◽  
Small Populations ◽  
Additive Effects ◽  
Steady Rate ◽  
Mutant Genes ◽  
Mutational Variance ◽  
Rate Of Response ◽  
Selection Of ◽  
New Mutations

SUMMARYThe influence of linkage on the rates of response to continued directional selection of quantitative traits deriving from variation contributed by new mutations in finite populations is investigated. Mutant genes are assumed to have additive effects which are randomly sampled from a symmetric distribution, and to be randomly located on the chromosome. Results were obtained by Monte Carlo simulation.The expected steady rate of response, when variability from new mutations is balanced by that lost by drift and selection, is reduced the tighter the linkage, but the reduction is small unless there are few, short chromosomes. For a given rate of new mutational variance per haploid chromosome set per generation, greater effects of linkage are obtained in large than in small populations, because more mutants segregate. The response and influence of linkage are essentially the same whether the new variance is due to many genes of small effect or few of large effect.The variability of response between replicates and generations was investigated, and the contribution to this of new mutants or recombination of existing mutants compared. Usually most genetic variability was due to the occurrence of a new favourable mutant of large effect.

Inbreeding reduces reproductive fitness

2017 ◽  
Author(s):  
Richard Frankham ◽  
Jonathan D. Ballou ◽  
Katherine Ralls ◽  
Mark D. B. Eldridge ◽  
Michele R. Dudash ◽  
...  
Keyword(s):  
Natural Selection ◽  
Inbreeding Depression ◽  
Reproductive Fitness ◽  
Heterozygote Advantage ◽  
Small Populations ◽  
Population Bottlenecks ◽  
Risk Of Extinction ◽  
Survival And Reproduction

The harmful impacts of inbreeding are generally greater in species that naturally outbreed compared to those in inbreeding species, greater in stressful than benign environments, greater for fitness than peripheral traits, and greater for total fitness compared to its individual components. Inbreeding reduces survival and reproduction (i.e., it causes inbreeding depression), and thereby increases the risk of extinction. Inbreeding depression is due to increased homozygosity for harmful alleles and at loci exhibiting heterozygote advantage. Natural selection may remove (purge) the alleles that cause inbreeding depression, especially following inbreeding or population bottlenecks, but it has limited effects in small populations and usually does not completely eliminate inbreeding depression. Inbreeding depression is nearly universal in sexually reproducing organisms that are diploid or have higher ploidies.

Evolutionary genetics of small populations

2017 ◽  
Author(s):  
Richard Frankham ◽  
Jonathan D. Ballou ◽  
Katherine Ralls ◽  
Mark D. B. Eldridge ◽  
Michele R. Dudash ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Population Size ◽  
Evolutionary Genetics ◽  
Small Population ◽  
Small Populations ◽  
Effective Population ◽  
Genetic Management ◽  
Evolutionary Genetic ◽  
Loss Of Genetic Diversity ◽  
Number Of Individuals

Genetic management of fragmented populations involves the application of evolutionary genetic theory and knowledge to alleviate problems due to inbreeding and loss of genetic diversity in small population fragments. Populations evolve through the effects of mutation, natural selection, chance (genetic drift) and gene flow (migration). Large outbreeding, sexually reproducing populations typically contain substantial genetic diversity, while small populations typically contain reduced levels. Genetic impacts of small population size on inbreeding, loss of genetic diversity and population differentiation are determined by the genetically effective population size, which is usually much smaller than the number of individuals.

scholarly journals Identification of new mutations in sterol 27-hydroxylase gene in Japanese patients with cerebrotendinous xanthomatosis (CTX).

1994 ◽  
Vol 35 (6) ◽  
pp. 1031-1039
Author(s):  
K S Kim ◽  
S Kubota ◽  
M Kuriyama ◽  
J Fujiyama ◽  
I Björkhem ◽  
...  
Keyword(s):  
Japanese Patients ◽  
Cerebrotendinous Xanthomatosis ◽  
Hydroxylase Gene ◽  
New Mutations

scholarly journals Mutational Analysis of a Histone Deacetylase in Drosophila melanogaster: Missense Mutations Suppress Gene Silencing Associated With Position Effect Variegation

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 657-668 ◽  
Author(s):  
Randy Mottus ◽  
Richard E Sobel ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Histone Deacetylase ◽  
Transcriptional Activity ◽  
Mutational Analysis ◽  
Position Effect ◽  
Transcriptional Regulator ◽  
Position Effect Variegation ◽  
Missense Mutations ◽  
Effect Variegation ◽  
New Mutations

Abstract For many years it has been noted that there is a correlation between acetylation of histones and an increase in transcriptional activity. One prediction, based on this correlation, is that hypomorphic or null mutations in histone deacetylase genes should lead to increased levels of histone acetylation and result in increased levels of transcription. It was therefore surprising when it was reported, in both yeast and fruit flies, that mutations that reduced or eliminated a histone deacetylase resulted in transcriptional silencing of genes subject to telomeric and heterochromatic position effect variegation (PEV). Here we report the first mutational analysis of a histone deacetylase in a multicellular eukaryote by examining six new mutations in HDAC1 of Drosophila melanogaster. We observed a suite of phenotypes accompanying the mutations consistent with the notion that HDAC1 acts as a global transcriptional regulator. However, in contrast to recent findings, here we report that specific missense mutations in the structural gene of HDAC1 suppress the silencing of genes subject to PEV. We propose that the missense mutations reported here are acting as antimorphic mutations that “poison” the deacetylase complex and propose a model that accounts for the various phenotypes associated with lesions in the deacetylase locus.

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