Measuring spontaneous deleterious mutation process

Kondrashov, Alexey S.

doi:10.1007/978-94-011-5210-5_16

Cited by 30 publications

(45 citation statements)

References 133 publications

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“…The observed deleterious mutation rate of 0.31 is below 1, which is predicted to be the minimum level at which sex may have evolved to eliminate deleterious mutations through recombination leading to epistatic selection (Kondrashov 1988(Kondrashov , 1998. The Binscy assay allows us to avoid one key criticism of other estimation techniques by providing concomitant sibling controls, but there are other complications that affect estimates in general, such as the occurrence of epistatic interactions and mutations affecting processes other than viability, that will make our rate an underestimate of the overall deleterious genomic mutation rate.…”

Section: Resultsmentioning

confidence: 99%

“…For example, U estimates in the model organism Drosophila melanogaster range from 0.01-1, with extensive ongoing debates on the correct value (Drake et al 1998;Lynch et al 1999;Fry 2001;Keightley & Eyre-Walker 2001;Kondrashov 2001;Garcia-Dorado & Caballero 2002;Rice 2002;Garcia-Dorado et al 2004). One of the main reasons for difficulties in determining U in D. melanogaster is inadequate experimental controls (Kondrashov 1998;Houle & Nuzhdin 2004). In the standard methods of measuring the accumulation of deleterious mutations over time in D. melanogaster, the comparative controls have in many cases been unreliable.…”

Section: Introductionmentioning

confidence: 99%

“…Examples of these controls include the original base stock, the most fit lines at the end of the experiment and base stocks frozen at the beginning of the experiment. Problems have arisen in controls because of contamination with other flies, low recovery of frozen stocks, and genetic changes in the base stock over time (Kondrashov 1998).…”

Section: Introductionmentioning

confidence: 99%

“…What is needed is an experimental design where deleterious mutations both do and do not accumulate in morphologically distinct siblings that have similar genetic backgrounds and are raised in identical environments (Kondrashov 1998). In this study, we will describe such an experimental design, the Binscy assay.…”

Section: Introductionmentioning

confidence: 99%

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Deleterious genomic mutation rate for viability inDrosophila melanogasterusing concomitant sibling controls

2005

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New deleterious mutations may reduce health and fitness and are involved in the evolution and maintenance of numerous biological processes. Hence, it is important to estimate the deleterious genomic mutation rate ( U ) in representative higher organisms. However, these estimated rates vary widely, mainly because of inadequate experimental controls. Here we describe an experimental design (the Binscy assay) with concomitant sibling controls and estimate U for viability in Drosophila melanogaster to be 0.31. This estimate, like most published studies, focuses on viability mutations and the overall deleterious genomic mutation rate would therefore be higher.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Deleterious genomic mutation rate for viability inDrosophila melanogasterusing concomitant sibling controls

2005

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“…Mutations are thought to arise primarily from DNA-replication errors, but can also result from faulty DNA repair, transcription-mediated mutation, and environmental and physiological agents (47,(94)(95)(96)(97)(98). The mutation rate in coding DNA per generation underlies a diverse set of evolutionary phenomena, including the evolution of sex, aging, recombination, mating systems, species extinctions, reproductive isolation, and speciation (30,99). Evidence to date has shown that the mutation rate in coding DNA varies among animals (95,100,101), and the rate itself can be subject to selective pressures (98,101,102).…”

Section: Germ-line Segregation and Mutation Ratesmentioning

confidence: 99%

Causes and evolutionary consequences of primordial germ-cell specification mode in metazoans

Whittle

Extavour

2017

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

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In animals, primordial germ cells (PGCs) give rise to the germ lines, the cell lineages that produce sperm and eggs. PGCs form in embryogenesis, typically by one of two modes: a likely ancestral mode wherein germ cells are induced during embryogenesis by cell-cell signaling (induction) or a derived mechanism whereby germ cells are specified by using germ plasm-that is, maternally specified germ-line determinants (inheritance). The causes of the shift to germ plasm for PGC specification in some animal clades remain largely unknown, but its repeated convergent evolution raises the question of whether it may result from or confer an innate selective advantage. It has been hypothesized that the acquisition of germ plasm confers enhanced evolvability, resulting from the release of selective constraint on somatic gene networks in embryogenesis, thus leading to acceleration of an organism's protein-sequence evolution, particularly for genes expressed at early developmental stages, and resulting in high speciation rates in germ plasm-containing lineages (denoted herein as the "PGCspecification hypothesis"). Although that hypothesis, if supported, could have major implications for animal evolution, our recent large-scale coding-sequence analyses from vertebrates and invertebrates provided important examples of genera that do not support the hypothesis of liberated constraint under germ plasm. Here, we consider reasons why germ plasm might be neither a direct target of selection nor causally linked to accelerated animal evolution. We explore alternate scenarios that could explain the repeated evolution of germ plasm and propose potential consequences of the inheritance and induction modes to animal evolutionary biology.germ line | preformation | epigenesis | primordial germ cell | spandrel P rimordial germ cells (PGCs) are specialized cells located in sexual organs of animals. These cells are central to reproduction because they give rise to the germ lines and, ultimately, the sperm and eggs. The PGCs typically arise during early embryogenesis by one of two distinct modes: (i) induction, wherein germ cells are induced by cell-cell signaling pathways (also known as epigenesis); or (ii) inheritance, wherein germ cells are formed by using germ plasm (a specialized cytoplasm containing proteins and RNAs needed for PGC formation), that is, maternally generated germ-line determinants that are "preformed" before embryogenesis begins (also known as preformation) (1-3). The induction mode appears to be the more prevalent mode in animals and occurs in basally branching lineages, and thus is the hypothesized ancestral mechanism of PGC specification, whereas inheritance comprises the likely derived state (1) (Fig. 1) (see SI Appendix, section 1 on the less parsimonious scenario that induction is the derived mode). Induction has been inferred based on microscopic data from most animal clades studied to date and has been experimentally shown to occur in a diverse range of organisms, including mammals (Mus musculus) (4-8), salamanders (...

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Deleterious transposable elements and the extinction of asexuals

2004

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The genomes of virtually all sexually reproducing species contain transposable elements. Although active elements generally transpose more rapidly than they are inactivated by mutation or excision, their number can be kept in check by purifying selection if its effectiveness becomes disproportionately greater as their copy number increases. In sexually reproducing species, such synergistic selection can result from ectopic crossing-over or from homologous recombination under negative epistasis. In addition, there may be controls on transposon activity that are associated with meiosis. Because a sexual lineage that abandons sex must lack such mechanisms, it may be driven to extinction by the unchecked proliferation of deleterious transposons inherited from its sexual progenitor. An important component of the evolutionary advantage of sex over asex may therefore lie in the ability of sex, despite facilitating the spread of deleterious elements within interbreeding populations, also to restrain their intragenomic proliferation.

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Measuring spontaneous deleterious mutation process

Cited by 30 publications

References 133 publications

Deleterious genomic mutation rate for viability inDrosophila melanogasterusing concomitant sibling controls

Deleterious genomic mutation rate for viability inDrosophila melanogasterusing concomitant sibling controls

Causes and evolutionary consequences of primordial germ-cell specification mode in metazoans

Deleterious transposable elements and the extinction of asexuals

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