Selfish genetic elements

Abstract

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].

Fig 1. George Williams' Adaptation and Natural Selection (1966) and Richard Dawkins' The Selfish Gene (1976) were instrumental in introducing the gene's-eye view to evolutionary biology.

Fig 2. Segregation distorters (here shown in red) get transmitted to >50% of the gametes.

Fig 3. Homing endonucleases can recognize a target sequence, cut it, and then use it own sequence as a template during double strand break repair.

This converts a heterozygote into a homozygote.

Fig 4. Transposable elements self-replicate through two main mechanisms: via an RNA intermediate ("copy-and-paste"; class 1) or straight excision-insertion ("cut-and-paste"; class 2).

Fig 5. Genetic conflicts often arise because not all genes are inherited in the same way.

Examples include cytoplasmic male sterility (see Selfish mitochondria). While mitochondrial and chloroplast genes are generally maternally inherited, B chromosomes can be preferentially transmitted through both males and females.

Fig 6. Igf2 is an example of genomic imprinting.

In mice, the insulin-like growth factor 2 gene, Igf2, which is linked to hormone production and increased offspring growth is paternally expressed (maternally silenced) and the insulin-like growth factor 2 receptor gene Igf2r, which binds the growth protein and so slows growth, is maternally expressed (paternally silenced). The offspring is normal sized when both genes are present, or both genes are absent. When the maternally expressed gene (Igf2r) is experimentally knocked out the offspring has an unusually large size, and when the paternally expressed gene (Igf2) is knocked out, the offspring is unusually small.

Fig 7. The simplest form of greenbeard mechanism.

An individual with the greenbeard allele preferentially helps a fellow greenbeard individual.