From Darwin to Derrida: Selfish Genes, Social Selves, and the Meanings of Life. By David Haig; Foreword by Daniel C. Dennett. Cambridge (Massachusetts): MIT Press. $39.95. xxx + 477 p.; ill.; index. ISBN: 9780262043786 (hc); 9780262358026 (eb). 2020.

2020 ◽  
Vol 95 (3) ◽  
pp. 247-248
Author(s):  
Michael Ruse
Keyword(s):  
Selfish Genes

scholarly journals Selfish Genes, Pleiotropy and the Origin of Recombination

Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 2089-2097 ◽  
Author(s):  
Jody Hey
Keyword(s):  
Natural Selection ◽  
Simple Model ◽  
Computer Simulations ◽  
Recombination Rate ◽  
Evolutionary Origin ◽  
Deleterious Mutations ◽  
Beneficial Mutations ◽  
Selfish Genes ◽  
Simple Interaction

Abstract If multiple linked polymorphisms are under natural selection, then conflicts arise and the efficiency of natural selection is hindered relative to the case of no linkage. This simple interaction between linkage and natural selection creates an opportunity for mutations that raise the level of recombination to increase in frequency and have an enhanced chance of fixation. This important finding by S. Otto and N. Barton means that mutations that raise the recombination rate, but are otherwise neutral, will be selectively favored under fairly general circumstances of multilocus selection and linkage. The effect described by Otto and Barton, which was limited to neutral modifiers, can also be extended to include all modifiers of recombination, both beneficial and deleterious. Computer simulations show that beneficial mutations that also increase recombination have an increased chance of fixation. Similarly, deleterious mutations that also decrease recombination have an increased chance of fixation. The results suggest that a simple model of recombination modifiers, including both neutral and pleiotropic modifiers, is a necessary explanation for the evolutionary origin of recombination.

Babies and bathwaters: attachment, neuroscience, evolution and the left

Soundings ◽  
2019 ◽  
Vol 73 (73) ◽  
pp. 111-128
Author(s):  
Graham Music
Keyword(s):  
Attachment Theory ◽  
Developmental Psychology ◽  
Huge Amount ◽  
Far Right ◽  
Interpersonal Neurobiology ◽  
Selfish Genes ◽  
The Social ◽  
Social Orders ◽  
Crucial Part ◽  
The Brain

This article challenges thinkers and activists on the left who are over-suspicious of ideas heralding from disciplines such as interpersonal neurobiology, attachment theory, developmental psychology, and perhaps especially, evolutionary theory. Although scepticism is frequently warranted, especially as such discourses are often co-opted for neoliberal or far right ends, there is much in all of them that melds well with critiques of hegemonic social orders, providing potential fuel for those working for social change. Much work, for example that of Amy Cuddy, can be interpreted both conservatively and progressively. Work from within an attachment theory paradigm can play a crucial part in the battle of ideas: it has a huge amount to teach about how to create a more humane and egalitarian world, and in countering neoliberal beliefs that humans are innately primarily aggressive, competitive or selfish, or have selfish genes. The days are now over when the biological, psychological and the social need to be pitted against each other. Rather, they now have to be seen as mutually constituted. The brain is a social organ, embedded, embodied, enactive and extended, in large part a reflection of the social conditions in which it grows.

Reason, rational contracts, and selfish genes

2019 ◽  
pp. 83-108
Author(s):  
John Collier ◽  
Michael Stingl
Keyword(s):  
Selfish Genes

Selfish genes: a green beard in the red fire ant

Nature ◽  
10.1038/29064 ◽  
1998 ◽  
Vol 394 (6693) ◽  
pp. 573-575 ◽  
Author(s):  
Laurent Keller ◽  
Kenneth G. Ross
Keyword(s):  
Fire Ant ◽  
Selfish Genes ◽  
Red Fire Ant

scholarly journals Genealogical evidence for epidemics of selfish genes

2002 ◽  
Vol 99 (17) ◽  
pp. 11265-11269 ◽  
Author(s):  
P. K. Ingvarsson ◽  
D. R. Taylor
Keyword(s):  
Selfish Genes

scholarly journals A parasitic selfish gene that affects host promiscuity

2013 ◽  
Vol 280 (1770) ◽  
pp. 20131875 ◽  
Author(s):  
Paulina Giraldo-Perez ◽  
Matthew R. Goddard
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Molecular Genetics ◽  
Sexual Behaviour ◽  
Evolutionary Dynamics ◽  
Homing Endonuclease ◽  
Mendelian Inheritance ◽  
Selfish Gene ◽  
Selfish Genes ◽  
Selfish Element ◽  
Host Behaviour

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.

scholarly journals Life and Death of Selfish Genes: Comparative Genomics Reveals the Dynamic Evolution of Cytoplasmic Incompatibility

2020 ◽  
Vol 38 (1) ◽  
pp. 2-15 ◽  
Author(s):  
Julien Martinez ◽  
Lisa Klasson ◽  
John J Welch ◽  
Francis M Jiggins
Keyword(s):  
Cytoplasmic Incompatibility ◽  
Gene Gain ◽  
Evolutionary Models ◽  
Loss Of Function ◽  
Genome Sequences ◽  
Life And Death ◽  
Selfish Genes ◽  
Wolbachia Genome ◽  
The Cross ◽  
Gain Loss

Abstract Cytoplasmic incompatibility is a selfish reproductive manipulation induced by the endosymbiont Wolbachia in arthropods. In males Wolbachia modifies sperm, leading to embryonic mortality in crosses with Wolbachia-free females. In females, Wolbachia rescues the cross and allows development to proceed normally. This provides a reproductive advantage to infected females, allowing the maternally transmitted symbiont to spread rapidly through host populations. We identified homologs of the genes underlying this phenotype, cifA and cifB, in 52 of 71 new and published Wolbachia genome sequences. They are strongly associated with cytoplasmic incompatibility. There are up to seven copies of the genes in each genome, and phylogenetic analysis shows that Wolbachia frequently acquires new copies due to pervasive horizontal transfer between strains. In many cases, the genes have subsequently acquired loss-of-function mutations to become pseudogenes. As predicted by theory, this tends to occur first in cifB, whose sole function is to modify sperm, and then in cifA, which is required to rescue the cross in females. Although cif genes recombine, recombination is largely restricted to closely related homologs. This is predicted under a model of coevolution between sperm modification and embryonic rescue, where recombination between distantly related pairs of genes would create a self-incompatible strain. Together, these patterns of gene gain, loss, and recombination support evolutionary models of cytoplasmic incompatibility.

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