Genetic conflicts: the usual suspects and beyond

McLaughlin, Richard N.; Malik, Harmit S.

doi:10.1242/jeb.148148

Cited by 132 publications

(132 citation statements)

References 170 publications

(158 reference statements)

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“…The centromere is positioned in a way that it can effectively orient the chromosome during meiosis I through microtubule attachment and the proper orientation of a chromosome has been shown to be advantageous for its transmission to the next generation [11]. This phenomenon has led to a model dubbed centromere drive, where the centromere that positions the chromosome in the best orientation is selected, and is thought to be responsible for rapid evolution of centromeric DNA as its length and sequence can bias its transmission [92, 93]. Centromere drive is believed not to cause direct negative fertility effects to females, however if it reduces the fertility in males, the centromeric proteins would require to adapt and restore male fertility [94].…”

Section: Key Figure Figurementioning

confidence: 99%

Transposable Element Domestication As an Adaptation to Evolutionary Conflicts

2017

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Transposable elements (TEs) are selfish genetic units that typically encode proteins that enable their proliferation in the genome and spread across individual hosts. Here we review a growing number of studies that suggest that TE proteins have often been coopted or ‘domesticated’ by their host as adaptations to a variety of evolutionary conflicts. In particular, TE-derived proteins have been recurrently repurposed as part of defense systems that protect prokaryotes and eukaryotes against the proliferation of infectious or invasive agents, including viruses and TEs themselves. We argue that the domestication of TE proteins may often be the only evolutionary path toward the mitigation of the cost incurred by their own selfish activities.

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Section: Key Figure Figurementioning

confidence: 99%

Transposable Element Domestication As an Adaptation to Evolutionary Conflicts

2017

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“…That sentiment has since begun to change. An appreciation for selfish genetic elements and the implications they have for the evolution of genetic systems, organismal design, and biodiversity is now part of mainstream thought in evolutionary theory (e.g., Burt & Trivers, ; Crespi & Nosil, ; Hurst & Werren, ; McLaughlin & Malik, ; Rice, ; Werren, ). Further, we now have detailed knowledge or indirect evidence of drivers from virtually every well‐studied system (Burt & Trivers, ; Jaenike, ), including a purported case of drive in great apes (Nam et al., ).…”

Section: The Meiotic Drive Model Of Hybrid Incompatibility: Theory Anmentioning

confidence: 99%

Selfish X chromosomes and speciation

Patten

2018

Molecular Ecology

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In two papers published at about the same time almost thirty years ago, Frank (Evolution, 45, 1991a, 262) and Hurst and Pomiankowski (Genetics, 128, 1991, 841) independently suggested that divergence of meiotic drive systems-comprising genes that cheat meiosis and genes that suppress this cheating-might provide a general explanation for Haldane's rule and the large X-effect in interspecific hybrids. Although at the time, the idea was met with skepticism and a conspicuous absence of empirical support, the tide has since turned. Some of the clearest mechanistic explanations we have for hybrid male sterility involve meiotic drive systems, and several other cases of hybrid sterility are suggestive of a role for meiotic drive. In this article, I review these ideas and their descendants and catalog the current evidence for the meiotic drive model of speciation. In addition, I suggest that meiotic drive is not the only intragenomic conflict to involve the X chromosome and contribute to hybrid incompatibility. Sexually and parentally antagonistic selection pressures can also pit the X chromosome and autosomes against each other. The resulting intragenomic conflicts should lead to co-evolution within populations and divergence between them, thus increasing the likelihood of incompatibilities in hybrids. I provide a sketch of these ideas and interpret some empirical patterns in the light of these additional X-autosome conflicts.

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“…Viruses also often encode proteins that subvert human immune mechanisms. Thus, pathogenic viruses can provide selective pressures for evolutionary adaptation of multiple features of human biology (101). Virus–human interactions have driven as much as 30% of human genome evolution since divergence from chimpanzees (38), and genetic variation among humans produces a wide variety of responses to viral infections.…”

Section: Introductionmentioning

confidence: 99%

“…Many studies have focused on immunity-related genes, such as human leukocyte antigen (HLA) genes or genes associated with induction or effector functions of antiviral interferons (IFNs). Indeed, such studies are duly warranted given the prominent role of immunity genes in defending against viruses, and that many immunity-related genes are, in humans, highly polymorphic (101). Alternatively, extensive use of unbiased whole-genome approaches, such as genome-wide association studies (GWASs), has identified potential susceptibility genes among patient cohorts afflicted with specific disease manifestations of viral infections.…”

Section: Introductionmentioning

confidence: 99%

Human Genetic Determinants of Viral Diseases

et al. 2017

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Much progress has been made in the identification of specific human gene variants that contribute to enhanced susceptibility or resistance to viral diseases. Herein we review multiple discoveries made with genome-wide or candidate gene approaches that have revealed significant insights into virus–host interactions. Genetic factors that have been identified include genes encoding virus receptors, receptor-modifying enzymes, and a wide variety of innate and adaptive immunity-related proteins. We discuss a range of pathogenic viruses, including influenza virus, respiratory syncytial virus, human immunodeficiency virus, human T cell leukemia virus, human papilloma virus, hepatitis B and C viruses, herpes simplex virus, norovirus, rotavirus, parvovirus, and Epstein-Barr virus. Understanding the genetic underpinnings that affect infectious disease outcomes should allow tailored treatment and prevention approaches in the future.

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Genetic conflicts: the usual suspects and beyond

Cited by 132 publications

References 170 publications

Transposable Element Domestication As an Adaptation to Evolutionary Conflicts

Transposable Element Domestication As an Adaptation to Evolutionary Conflicts

Selfish X chromosomes and speciation

Human Genetic Determinants of Viral Diseases

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