A parasitic selfish gene that affects host promiscuity

Selfish genes demonstrate transmission bias and invade sexual populations despite conferring no benefit to their hosts. While the molecular genetics and evolutionary dynamics of selfish genes are reasonably well characterized, their effects on hosts are not. Homing endonuclease genes (HEGs) are one well-studied family of selfish genes that are assumed to be benign. However, we show that carrying HEGs is costly for Saccharomyces cerevisiae , demonstrating that these genetic elements are not necessarily benign but maybe parasitic. We estimate a selective load of approximately 1–2% in ‘natural’ niches. The second aspect we examine is the ability of HEGs to affect hosts' sexual behaviour. As all selfish genes critically rely on sex for spread, then any selfish gene correlated with increased host sexuality will enjoy a transmission advantage. While classic parasites are known to manipulate host behaviour, we are not aware of any evidence showing a selfish gene is capable of affecting host promiscuity. The data presented here show a selfish element may increase the propensity of its eukaryote host to undergo sex and along with increased rates of non-Mendelian inheritance, this may counterbalance mitotic selective load and promote spread. Demonstration that selfish genes are correlated with increased promiscuity in eukaryotes connects with ideas suggesting that selfish genes promoted the evolution of sex initially.

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Maternal effect killing by a supergene controlling ant social organization

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2003282117 ◽

2020 ◽

Vol 117 (29) ◽

pp. 17130-17134

Author(s):

Amaury Avril ◽

Jessica Purcell ◽

Sébastien Béniguel ◽

Michel Chapuisat

Keyword(s):

Social Organization ◽

Maternal Effect ◽

Evolutionary Dynamics ◽

Mendelian Inheritance ◽

Transmission Ratio Distortion ◽

Gene Drive ◽

Biological Organization ◽

Evolutionary Mechanisms ◽

Selfish Gene ◽

Selfish Genetic Element

Supergenes underlie striking polymorphisms in nature, yet the evolutionary mechanisms by which they arise and persist remain enigmatic. These clusters of linked loci can spread in populations because they captured coadapted alleles or by selfishly distorting the laws of Mendelian inheritance. Here, we show that the supergene haplotype associated with multiple-queen colonies in Alpine silver ants is a maternal effect killer. All eggs from heterozygous queens failed to hatch when they did not inherit this haplotype. Hence, the haplotype specific to multiple-queen colonies is a selfish genetic element that enhances its own transmission by causing developmental arrest of progeny that do not carry it. At the population level, such transmission ratio distortion favors the spread of multiple-queen colonies, to the detriment of the alternative haplotype associated with single-queen colonies. Hence, selfish gene drive by one haplotype will impact the evolutionary dynamics of alternative forms of colony social organization. This killer hidden in a social supergene shows that large nonrecombining genomic regions are prone to cause multifarious effects across levels of biological organization.

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Molecular genetics of met17 and met25 mutants of Saccharomyces cerevisiae: Intragenic complementation between mutations of a single structural gene

MGG Molecular & General Genetics ◽

10.1007/bf00331505 ◽

1987 ◽

Vol 207 (1) ◽

pp. 165-170 ◽

Cited By ~ 13

Author(s):

Richard D'Andrea ◽

Yolande Surdin-Kerjan ◽

Glenn Pure ◽

Hélène Cherest

Keyword(s):

Saccharomyces Cerevisiae ◽

Molecular Genetics ◽

Structural Gene ◽

Intragenic Complementation

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Comparative genomics and evolutionary dynamics of Saccharomyces cerevisiae Ty elements

Transposable Elements and Genome Evolution ◽

10.1007/978-94-011-4156-7_2 ◽

2000 ◽

pp. 3-13 ◽

Cited By ~ 1

Author(s):

King Jordan ◽

John F. McDonald

Keyword(s):

Saccharomyces Cerevisiae ◽

Comparative Genomics ◽

Evolutionary Dynamics ◽

Ty Elements

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Epidemic cycles driven by host behaviour

Journal of The Royal Society Interface ◽

10.1098/rsif.2014.0575 ◽

2014 ◽

Vol 11 (99) ◽

pp. 20140575 ◽

Cited By ~ 16

Author(s):

Benjamin M. Althouse ◽

Laurent Hébert-Dufresne

Keyword(s):

Sexual Behaviour ◽

Disease Transmission ◽

Control Strategies ◽

Treponema Pallidum ◽

Structured Populations ◽

Behavioural Interventions ◽

Sexually Transmitted ◽

The Face ◽

The Usa ◽

Host Behaviour

Host immunity and demographics (the recruitment of susceptibles via birthrate) have been demonstrated to be a key determinant of the periodicity of measles, pertussis and dengue epidemics. However, not all epidemic cycles are from pathogens inducing sterilizing immunity or are driven by demographics. Many sexually transmitted infections are driven by sexual behaviour. We present a mathematical model of disease transmission where individuals can disconnect and reconnect depending on the infectious status of their contacts. We fit the model to historic syphilis ( Treponema pallidum ) and gonorrhea ( Neisseria gonorrhoeae ) incidence in the USA and explore potential intervention strategies against syphilis. We find that cycles in syphilis incidence can be driven solely by changing sexual behaviour in structured populations. Our model also explains the lack of similar cycles in gonorrhea incidence even if the two infections share the same propagation pathways. Our model similarly illustrates how sudden epidemic outbreaks can occur on time scales smaller than the characteristic demographic time scale of the population and that weaker infections can lead to more violent outbreaks. Behaviour also appears to be critical for control strategies as we found a bigger sensitivity to behavioural interventions than antibiotic treatment. Thus, behavioural interventions may play a larger role than previously thought, especially in the face of antibiotic resistance and low intervention efficacies.

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Selection response in traits with maternal inheritance

Genetics Research ◽

10.1017/s0016672300025520 ◽

1990 ◽

Vol 55 (3) ◽

pp. 189-197 ◽

Cited By ~ 83

Author(s):

Russell Lande ◽

Mark Kirkpatrick

Keyword(s):

Artificial Selection ◽

Evolutionary Dynamics ◽

Maternal Inheritance ◽

Natural Populations ◽

Mendelian Inheritance ◽

Time Lags ◽

Response To Selection ◽

Paternal Effects ◽

Practical Applications ◽

Economic Improvement

SummaryMaternal inheritance is the non-Mendelian transmission of traits, from mothers to their offspring. Despite its presence in virtually all organisms, acting through a variety of mechanisms, the evolutionary consequences of maternal inheritance are not well understood. Here we review and extend a model of the inheritance and evolution of multiple quantitative characters with complex pathways of maternal effects. Extensions of the earlier model include common family environmental effects not associated with maternal phenotype, sexual dimorphism, and paternal effects (non-Mendelian influence of the father on offspring traits). We find that, in contrast to simple Mendelian inheritance, maternal inheritance produces qualitatively different evolutionary dynamics for two reasons: (1) the response to selection on a set of characters depends not only on their additive genetic variances and covariances, but also on maternal characters that influence them, and (2) time lags in the response to selection create a form of evolutionary momentum. These results have important implications for evolution in natural populations and practical applications in the economic improvement of domesticated species. We derive selection indices that maximize either the economic improvement in a single generation of artificial selection or the asymptotic rate of improvement in long-term selection programmes, based on individual merit or a combination of individual and family merit. Numerical examples show that accounting for maternal inheritance can lead to considerable increases in the efficiency of artificial selection.

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Killer systems in Saccharomyces cerevisiae: three distinct modes of exclusion of M2 double-stranded RNA by three species of double-stranded RNA, M1, L-A-E, and L-A-HN.

Molecular and Cellular Biology ◽

10.1128/mcb.3.4.654 ◽

1983 ◽

Vol 3 (4) ◽

pp. 654-661 ◽

Cited By ~ 28

Author(s):

R B Wickner

Keyword(s):

Saccharomyces Cerevisiae ◽

Killer Toxin ◽

Mendelian Inheritance ◽

Double Stranded Rna ◽

Heat Curing ◽

Natural Variants

M1 and M2 double-stranded RNAs (dsRNAs) code for the K1R1 and K2R2 killer toxin and resistance functions, respectively. Natural variants of a larger dsRNA (L-A) carry various combinations of the [EXL], [HOK], and [NEX] genes, which affect the K1 and K2 killer systems. Other dsRNAs, the same size as L-A, called L-B and L-C, are often present with L-A. We show that K1 killer strains have [HOK] and [NEX] but not [EXL] on their L-A (in disagreement with Field et al., Cell 31:193-200, 1982). These strains also carry other L-size molecules detectable after heat-curing has eliminated L-A. The exclusion of M2 dsRNA observed on mating K2 strains with K1 strains is due to the M1 dsRNA (not the L-A dsRNA as claimed by Field et al.) in the K1 strains. Four independent mutants of a [KIL-k2] [NEX-o] [HOK-o] strain were selected for resistance to [EXL] exclusion of M2 ([EXLR] phenotype). The [EXLR] phenotype showed non-Mendelian inheritance in each case, and these mutants had simultaneously each acquired [HOK]. The mutations were located on L-A and not on M2, and did not confer resistance to M1 exclusion of M2.

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The selfish goal meets the selfish gene

Behavioral and Brain Sciences ◽

10.1017/s0140525x13002136 ◽

2014 ◽

Vol 37 (2) ◽

pp. 153-154

Author(s):

Steven L. Neuberg ◽

Mark Schaller

Keyword(s):

Human Cognition ◽

Evolutionary Perspective ◽

Motivational Systems ◽

Selfish Gene ◽

Selfish Genes ◽

And Behavior

AbstractThe connection between selfish genes and selfish goals is not merely metaphorical. Many goals that shape contemporary cognition and behavior are psychological products of evolutionarily fundamental motivational systems and thus are phenotypic manifestations of genes. An evolutionary perspective can add depth and nuance to our understanding of “selfish goals” and their implications for human cognition and behavior.

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Selfish Genes and Social Darwinism

Philosophy ◽

10.1017/s0031819100068431 ◽

1983 ◽

Vol 58 (225) ◽

pp. 365-377 ◽

Cited By ~ 11

Author(s):

Mary Midgley

Keyword(s):

Sudden Death ◽

Time Lag ◽

Social Darwinism ◽

Selfish Gene ◽

Selfish Genes ◽

Andromeda Nebula

Exchanging views in Philosophy with a two-year time-lag is getting rather like conversation with the Andromeda Nebula. I am distressed that my reply to Messrs Mackie and Dawkins, explaining what made me write so crossly about The Selfish Gene, has been so long delayed. Mr Mackie's sudden death in December 1981 adds a further dimension to this distress.

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