Selfish Genes Research Articles

A New Feudalism: Selfish Genes, Great Wealth and the Rise of the Dynastic Family Trust

Today’s record levels of economic inequality are infecting our future as the top 0.01% bequest vast wealth to their descendants. With the death of the Rule Against Perpetuities (RAP), this inequality has the potential to harden social class lines not just for a generation or two but forever. Although it may sound implausible, interviews with estate lawyers serving very high net worth clients reveal that some of the wealthiest tier of testators are already exploiting the RAP’s elimination, along with a tax loophole, to establish dynasty trusts that will financially empower their bloodline as long as it continues. Evolutionary biologists will not be surprised by this finding. Recent work in their field shows a universal and powerful human drive for high status descendants — a drive for “quality” progeny so powerful that it appears to trump the usual desire to maximize quantity of offspring. Coupled with the long history of dynastic family wealth in England, this science suggests that today’s wealthiest testators will utilize powerful modern legal institutions (e.g. well-developed laws of contract and trust; deep and efficient capital markets) to forge a new sort of trust that I dub a Dynastic Family Trusts (DFT). These DFTs will be larded with innovative provisions leveraging a founder’s wealth to maximize descendants’ status for generation after generation. For those fearing the pernicious effects of concentrated wealth on democracy and equal opportunity, the rise of the DFT is alarming. Fortunately there is a very easy fix: simply reinstate the Rule Against Perpetuities. Given a race-to-the-bottom dynamic among the states, national legislation from Congress is necessary.

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

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.

'Bacterial Programmed Cell Death': cellular altruism or genetic selfism?

Cell-dependent propagation of the 'self' is the driver of all species, organisms and even genes. Conceivably, elimination of these entities is caused by cellular death. Then, how can genes that cause the death of the same cell evolve? Programmed cell death (PCD) is the gene-dependent self-inflicted death. In multicellular organisms, PCD of a cell confers fitness to the surviving rest of the organism, which thereby allows the selection of genes responsible for PCD. However, PCD in free-living bacteria is intriguing; the death of the cell is the death of the organism. How can such PCD genes be selected in unicellular organisms? The bacterial PCD in a population is proposed to confer fitness to the surviving kin in the form of sporulation, nutrition, infection-containment and matrix materials. While the cell-centred view leading to propositions of 'altruism' is enticing, the gene-centred view of 'selfism' is neglected. In this opinion piece, we reconceptualize the PCD propositions as genetic selfism (death due to loss/mutation of selfish genes) rather than cellular altruism (death for the conferment of fitness to kin). Within the scope and the available evidence, we opine that some of the PCD-like observations in bacteria seem to be the manifestation of genetic selfism by Restriction-Modification systems and Toxin-Antitoxin systems.

Introduction to Evolutionary Developmental Pathology, or Evo-Devo-Path: on Neodarwinism, Natural Mutants, Hopeful Monsters, Syndromes, Genomics, Variations, Humans, Apes, Chameleons, and Dinosaurs

During the second half of the twentieth century, few authors attempted to combine the increasing knowledge obtained from the study of model organisms and human medicine with data from comparative anatomy, evolutionary biology, “natural mutants,” and variations in order to investigate the links between development, pathology, and macroevolution. However, in the last decades, there has been a renewed interest on these subjects, with the rise of Evolutionary Developmental Pathology (Evo-Devo-Path), a field that is attracting more and more attention across the globe, not only from the scientific community but also from the media and broader public. This is because this field is mainly related to a deeper understanding of developmental anomalies and disease within an evolutionary framework, paying a special attention to “natural mutants,” such as cyclopic sheep, humans with severe congenital malformations, and to so-called “hopeful monsters,” such as chameleons and, to a certain extent, dinosaurs, as will be explained in this issue. These are hot topics within the broader community and for the media, that have been also of main interest to biologists for a long time, for instance to renowned authors such as Etienne Geoffroy Saint-Hilaire, Waddington, Goldschmidt, Gould and Per Alberch. However, these issues became somewhat neglected with the rise of genetics and the increased focus on the “Devo” within Evolutionary Developmental Biology (Evo-Devo), in particular on molecular biology studies and therefore on experimentally produced—and not so much on “natural”—mutations. Another main, and related, reason was the prevalence of Neodarwinism within biology—sometimes defended in a quasi-religious way and using extremist ideas, such as reducing evolution to “selfish genes,” that, we now know, do not correspond to the complex and multifaceted reality of biological evolution within this planet. These subjects will be discussed in this special, and very timely, issue precisely about Evo-Devo-Path, which attests the increasing interest in this field, and thus on natural mutants, “hopeful monsters,” and other ideas of the authors named just above, and shows how new knowledge and tools, for instance about the cardiopharyngeal muscles and syndromes and about genomics and transposable elements, are quickly being integrated in crucial discussions within this field.

Selfish genes and sexual selection: the impact of genomic parasites on host reproduction

AbstractSelfish genetic elements (SGEs) such as replicating mobile elements, segregation distorters and maternally inherited endosymbionts, bias their transmission success relative to the rest of the genome to increase in representation in subsequent generations. As such, they generate conflict with the rest of the genome. Such intragenomic conflict is also a hallmark of sexually antagonistic (SA) alleles, which are shared genes between the sexes but that have opposing fitness effects when expressed in males and females. However, whilst both SGEs and SA alleles are recognized as common and potent sources of genomic conflict, the realization that SGEs can also generate sexually antagonistic selection and contribute to sexual conflict in addition to generate sexual selection is largely overlooked. Here, I show that SGEs frequently generate sex‐specific selection and outline how SGEs that are associated with compromised male fertility can shape female mating patterns, play a key role in the dynamics of sex‐determination systems and likely be an important source of sexually antagonistic genetic variation. Given the prevalence of SGEs, their contribution to sexual conflict is likely to be greatly overlooked.

Dramatically diverse Schizosaccharomyces pombe wtf meiotic drivers all display high gamete-killing efficiency.

Meiotic drivers are selfish alleles that can force their transmission into more than 50% of the viable gametes made by heterozygotes. Meiotic drivers are known to cause infertility in a diverse range of eukaryotes and are predicted to affect the evolution of genome structure and meiosis. The wtf gene family of Schizosaccharomyces pombe includes both meiotic drivers and drive suppressors and thus offers a tractable model organism to study drive systems. Currently, only a handful of wtf genes have been functionally characterized and those genes only partially reflect the diversity of the wtf gene family. In this work, we functionally test 22 additional wtf genes for meiotic drive phenotypes. We identify eight new drivers that share between 30–90% amino acid identity with previously characterized drivers. Despite the vast divergence between these genes, they generally drive into >85% of gametes when heterozygous. We also identify three wtf genes that suppress other wtf drivers, including two that also act as autonomous drivers. Additionally, we find that wtf genes do not underlie a weak (64% allele transmission) meiotic driver on chromosome 1. Finally, we find that some Wtf proteins have expression or localization patterns that are distinct from the poison and antidote proteins encoded by drivers and suppressors, suggesting some wtf genes may have non-meiotic drive functions. Overall, this work expands our understanding of the wtf gene family and the burden selfish driver genes impose on S. pombe.

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

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.

The molecular biology of the elites is replaced by an environmentally interactive biology of social equality

What is life, and ultimately human nature and its biology? The answer to these questions requires a close examination of the scientific validity of the widespread gene-centred notion of human nature’s blind dependence on ‘selfish genes’. This perception has been imposed on biological science and eventually on the public by the economic elites since the 1920s, with the creation of Molecular Biology in order to scientifically justify their economic-political power as inherently (genetically) predetermined. However, new scientific developments in biology have questioned this perception, and redefine human nature as the result of biochemical interactions, feedback and modulation mechanisms between life’s different levels of organization (cells, organs, organism) with the environment, physical and social. DNA is acting as a passive library of stored genetic information provided on demand by the organisms, and man, in response of their adaptive requirements to their intra-/inter-organisms’ environment, and also to the external (physical, social) environment, which life itself modifies in response. The present study expands the scientific arguments of a previous critique of Marx and Marxism on its acceptance of genetic inequality among humans, for the main reason that this unscientific notion and centrepiece of the ideology of the economic elites pervades and the core of the ideology of the communist, left and anarchist fragmentations of Marxism. The new scientific evidence clearly shows that the biology of man necessitates that for his survival as species he should organize socio-political structures comprised of individuals unconditionally recognized as biologically and intellectually equivalent from birth. The new science of Biology is presented here extensively and in layman’s terms with the wish to be considered by scientific study groups formulated in each and every political fragmentation of the left to help converge into a new unifying ideology of unconditional equality among men. Such ideology should be fully depleted from any elements of the gene-centred ideology of the capitalist elites as to be clearly recognized and contrasted by the masses, in order to help them realize that they are viewed by the elites as genetically inferior and degenerate disposables, with the aim to give them a clearer purpose to react against them.

Selfish genetic elements.

Selfish genetic elements (historically also referred to as selfish genes, ultra-selfish genes, selfish DNA, parasitic DNA, genomic outlaws) are genetic segments that can enhance their own transmission at the expense of other genes in the genome, even if this has no or a negative effect on organismal fitness. [1–6] Genomes have traditionally been viewed as cohesive units, with genes acting together to improve the fitness of the organism. However, when genes have some control over their own transmission, the rules can change, and so just like all social groups, genomes are vulnerable to selfish behaviour by their parts. Early observations of selfish genetic elements were made almost a century ago, but the topic did not get widespread attention until several decades later. Inspired by the gene-centred views of evolution popularized by George Williams[7] and Richard Dawkins,[8] two papers were published back-to-back in Nature in 1980—by Leslie Orgel and Francis Crick[9] and Ford Doolittle and Carmen Sapienza[10] respectively—introducing the concept of selfish genetic elements (at the time called “selfish DNA”) to the wider scientific community. Both papers emphasized that genes can spread in a population regardless of their effect on organismal fitness as long as they have a transmission advantage. Selfish genetic elements have now been described in most groups of organisms, and they demonstrate a remarkable diversity in the ways by which they promote their own transmission.[11] Though long dismissed as genetic curiosities, with little relevance for evolution, they are now recognized to affect a wide swath of biological processes, ranging from genome size and architecture to speciation.[12]

Botulinum Neurotoxin Diversity from a Gene-Centered View.

Botulinum neurotoxins (BoNTs) rank amongst the most potent toxins known. The factors responsible for the emergence of the many known and yet unknown BoNT variants remain elusive. It also remains unclear why anaerobic bacteria that are widely distributed in our environment and normally do not pose a threat to humans, produce such deadly toxins. Even the possibility of accidental toxicity to humans has not been excluded. Here, I review the notion that BoNTs may have specifically evolved to target vertebrates. Considering the extremely complex molecular architecture of the toxins, which enables them to reach the bloodstream, to recognize and enter neurons, and to block neurotransmitter release, it seems highly unlikely that BoNT toxicity to vertebrates is a coincidence. The carcass–maggot cycle provides a plausible explanation for a natural role of the toxins: to enable mass reproduction of bacteria, spores, and toxins, using toxin-unaffected invertebrates, such as fly maggots, as the vectors. There is no clear correlation between toxigenicity and a selective advantage of clostridia in their natural habitat. Possibly, non-toxigenic strains profit from carcasses resulting from the action of toxigenic strains. Alternatively, a gene-centered view of toxin evolution would also explain this observation. Toxin-coding mobile genetic elements may have evolved as selfish genes, promoting their own propagation, similar to commensal viruses, using clostridia and other bacteria as the host. Research addressing the role of BoNTs in nature and the origin of toxin variability goes hand in hand with the identification of new toxin variants and the design of improved toxin variants for medical applications. These research directions may also reveal yet unknown natural antidotes against these extremely potent neurotoxins.

The PIWI-Interacting RNA Molecular Pathway: Insights From Cultured Silkworm Germline Cells.

The PIWI-interacting RNA (piRNA) pathway, one of the major eukaryotic small RNA silencing pathways, is a genome surveillance system that silences selfish genes in animal gonads. piRNAs guide PIWI protein to target genes through Watson-Crick RNA-RNA base-parings. Loss of piRNA function causes genome instability, inducing failure in gametogenesis and infertility. Studies using fruit flies and mice as key experimental models have resulted in tremendous progress in understanding the mechanism underlying the piRNA pathway. Recent work using cultured silkworm germline cells has also expanded our knowledge of piRNA biogenesis in particular, since these silkworm cells are the only cells of germline origin that can be cultured. In this review, we describe elucidation of the piRNA pathway using cultured silkworm cells as an experimental model by focusing on recent work in biochemistry and structural biology. Earlier studies that made important contributions to the field are also described.

How selfish genes get their way

Meiotic Drive At the core of Mendelian genetics is the concept that gametes are equally likely to carry either of the two parental copies of a gene. Selfish genetic elements can cheat, however, by subverting Mendelian segregation to increase their representation in the gametes. Akera et al. show how the inherent asymmetry of female meiosis is translated to an asymmetry within the spindle machinery that segregates the chromosomes (see the Perspective by McNally). Experiments in mouse eggs revealed how asymmetry is exploited by selfish genetic elements to increase their transmission to the egg. Science , this issue p. [668][1]; see also p. [594][2] [1]: /lookup/doi/10.1126/science.aan0092 [2]: /lookup/doi/10.1126/science.aaq0200

Wtf genes are prolific dual poison-antidote meiotic drivers

Meiotic drivers are selfish genes that bias their transmission into gametes, defying Mendelian inheritance. Despite the significant impact of these genomic parasites on evolution and infertility, few meiotic drive loci have been identified or mechanistically characterized. Here, we demonstrate a complex landscape of meiotic drive genes on chromosome 3 of the fission yeasts Schizosaccharomyces kambucha and S. pombe. We identify S. kambucha wtf4 as one of these genes that acts to kill gametes (known as spores in yeast) that do not inherit the gene from heterozygotes. wtf4 utilizes dual, overlapping transcripts to encode both a gamete-killing poison and an antidote to the poison. To enact drive, all gametes are poisoned, whereas only those that inherit wtf4 are rescued by the antidote. Our work suggests that the wtf multigene family proliferated due to meiotic drive and highlights the power of selfish genes to shape genomes, even while imposing tremendous costs to fertility.

X chromosome drive in a widespread Palearctic woodland fly, Drosophila testacea.

Selfish genes that bias their own transmission during meiosis can spread rapidly in populations, even if they contribute negatively to the fitness of their host. Driving X chromosomes provide a clear example of this type of selfish propagation. These chromosomes have important evolutionary and ecological consequences, and can be found in a broad range of taxa including plants, mammals and insects. Here, we report a new case of X chromosome drive (X drive) in a widespread woodland fly, Drosophila testacea. We show that males carrying the driving X (SR males) sire 80-100% female offspring and possess a diagnostic X chromosome haplotype that is perfectly associated with the sex ratio distortion phenotype. We find that the majority of sons produced by SR males are sterile and appear to lack a Y chromosome, suggesting that meiotic defects involving the Y chromosome may underlie X drive in this species. Abnormalities in sperm cysts of SR males reflect that some spermatids are failing to develop properly, confirming that drive is acting during gametogenesis. By screening wild-caught flies using progeny sex ratios and a diagnostic marker, we demonstrate that the driving X is present in wild populations at a frequency of ~10% and that suppressors of drive are segregating in the same population. The testacea species group appears to be a hot spot for X drive, and D.testacea is a promising model to compare driving X chromosomes in closely related species, some of which may even be younger than the chromosomes themselves.

Thought Experiments and the Ostia of Paranasal Sinuses

It behooves us to understand the power of gravity or its diminished or negative effect as we, Homo sapiens, evolve from going around from four limbs to bipedalism or working mostly erect or sitting on our buttocks. Evolution doesn’t favor a particular desire or anticipate the future; its particular end is to get that individual to live long and propagate more efficiently. Evolution cannot give you all the favorable advantages; only that selfish genes will make us the top predators. Unfortunately the locations of the paranasal sinus ostia are not top in the list of favorable advantages. Hemorrhoids, chronic back pain, varicous veins, etc are other morbid consequences of bipedalism.

Genetically Modified Aedes aegypti to Control Dengue: A Review.

Dengue is an acute infectious disease of viral etiology characterized by lymphadenopathy, leucopenia, headache, biphasic fever, pain in various parts of the body, rashes, and extreme physical weakness. It is a vector-borne disease caused by a positive-stranded RNA virus of the family Flaviviridae, genus Flavivirus. Dengue inflicts a significant health, economic, and social burden on populations of endemic areas. Dengue virus is transmitted to humans by the mosquito vector Aedes aegypti. Vaccines against dengue viruses have been claimed to be developed, but as yet no effective treatment is available. Alternative therapeutic strategies to overcome this disease and its spread are direly needed. A traditional sterile insect technique (SIT) harms the health of male insects, leading to their reduced ability to compete for wild-type female insects for breeding. Oxitec (Abingdon, UK) has developed genetically modified (GM) strains of A. aegypti via the release of insects carrying a dominant lethal (RIDL) strategy. RIDL male mosquitoes offer a resolution to many of the limitations of traditional SIT, which has resulted in reduced application of SIT in mosquitoes. The technique using RIDL mosquitoes is considered to be ecologically friendly and specific. Homing endonuclease genes, also called selfish genes, can also be used in genetic modification methods in such a way that the vector population and its competency can be reduced. GM mosquitoes carrying a gene that transcribes RNA interference can also be crucial to control expression of RNA viruses. The RNA virus interference pathway is one of the most critical components of the innate immune system of insects that can frustrate a variety of RNA viruses such as Flaviviruses. Here, we summarize and focus on alternative techniques used to control dengue spread.

Fruiting Body Formation in Volvariella volvacea Can Occur Independently of Its MAT-A-Controlled Bipolar Mating System, Enabling Homothallic and Heterothallic Life Cycles.

Volvariella volvacea is an important crop in Southeast Asia, but erratic fruiting presents a serious challenge for its production and breeding. Efforts to explain inconsistent fruiting have been complicated by the multinucleate nature, typical lack of clamp connections, and an incompletely identified sexual reproductive system. In this study, we addressed the life cycle of V. volvacea using whole genome sequencing, cloning of MAT loci, karyotyping of spores, and fruiting assays. Microscopy analysis of spores had previously indicated the possible coexistence of heterothallic and homothallic life cycles. Our analysis of the MAT loci showed that only MAT-A, and not MAT-B, controlled heterokaryotization. Thus, the heterothallic life cycle was bipolar. Karyotyping of single spore isolates (SSIs) using molecular markers supported the existence of heterokaryotic spores. However, most SSIs were clearly not heterokaryotic, yet contained structural variation (SV) markers relating to both alleles of both parents. Heterokaryons from crossed, self-sterile homokaryons could produce fruiting bodies, agreeing with bipolar heterothallism. Meanwhile, some SSIs with two different MAT-A loci also produced fruiting bodies, which supported secondary homothallism. Next, SSIs that clearly contained only one MAT-A locus (homothallism) were also able to fruit, demonstrating that self-fertile SSIs were not, per definition, secondary homothallic, and that a third life cycle or genetic mechanism must exist. Finally, recombination between SV markers was normal, yet 10 out of 24 SV markers showed 1:2 or 1:3 distributions in the spores, and large numbers of SSIs contained doubled SV markers. This indicated selfish genes, and possibly partial aneuploidy.

Forty years of The Selfish Gene are not enough.

Forty years of The Selfish Gene are not enough.

R2d2 Drives Selfish Sweeps in the House Mouse.

A selective sweep is the result of strong positive selection driving newly occurring or standing genetic variants to fixation, and can dramatically alter the pattern and distribution of allelic diversity in a population. Population-level sequencing data have enabled discoveries of selective sweeps associated with genes involved in recent adaptations in many species. In contrast, much debate but little evidence addresses whether “selfish” genes are capable of fixation—thereby leaving signatures identical to classical selective sweeps—despite being neutral or deleterious to organismal fitness. We previously described R2d2, a large copy-number variant that causes nonrandom segregation of mouse Chromosome 2 in females due to meiotic drive. Here we show population-genetic data consistent with a selfish sweep driven by alleles of R2d2 with high copy number (R2d2HC) in natural populations. We replicate this finding in multiple closed breeding populations from six outbred backgrounds segregating for R2d2 alleles. We find that R2d2HC rapidly increases in frequency, and in most cases becomes fixed in significantly fewer generations than can be explained by genetic drift. R2d2HC is also associated with significantly reduced litter sizes in heterozygous mothers, making it a true selfish allele. Our data provide direct evidence of populations actively undergoing selfish sweeps, and demonstrate that meiotic drive can rapidly alter the genomic landscape in favor of mutations with neutral or even negative effects on overall Darwinian fitness. Further study will reveal the incidence of selfish sweeps, and will elucidate the relative contributions of selfish genes, adaptation and genetic drift to evolution.

Origin, evolution, and population genetics of the selfish Segregation Distorter gene duplication in European and African populations of Drosophila melanogaster.

Meiotic drive elements are a special class of evolutionarily "selfish genes" that subvert Mendelian segregation to gain preferential transmission at the expense of homologous loci. Many drive elements appear to be maintained in populations as stable polymorphisms, their equilibrium frequencies determined by the balance between drive (increasing frequency) and selection (decreasing frequency). Here we show that a classic, seemingly balanced, drive system is instead characterized by frequent evolutionary turnover giving rise to dynamic, rather than stable, equilibrium frequencies. The autosomal Segregation Distorter (SD) system of the fruit fly Drosophila melanogaster is a selfish coadapted meiotic drive gene complex in which the major driver corresponds to a partial duplication of the gene Ran-GTPase activating protein (RanGAP). SD chromosomes segregate at similar, low frequencies of 1-5% in natural populations worldwide, consistent with a balanced polymorphism. Surprisingly, our population genetic analyses reveal evidence for parallel, independent selective sweeps of different SD chromosomes in populations on different continents. These findings suggest that, rather than persisting at a single stable equilibrium, SD chromosomes turn over frequently within populations.