Academic journal article Genetics

Genetic Addiction: Selfish Gene's Strategy for Symbiosis in the Genome

Academic journal article Genetics

Genetic Addiction: Selfish Gene's Strategy for Symbiosis in the Genome

Article excerpt

ABSTRACT

The evolution and maintenance of the phenomenon of postsegregational host killing or genetic addiction are paradoxical. In this phenomenon, a gene complex, once established in a genome, programs death of a host cell that has eliminated it. The intact form of the gene complex would survive in other members of the host population. It is controversial as to why these genetic elements are maintained, due to the lethal effects of host killing, or perhaps some other properties are beneficial to the host. We analyzed their population dynamics by analytical methods and computer simulations. Genetic addiction turned out to be advantageous to the gene complex in the presence of a competitor genetic element. The advantage is, however, limited in a population without spatial structure, such as that in a well-mixed liquid culture. In contrast, in a structured habitat, such as the surface of a solid medium, the addiction gene complex can increase in frequency, irrespective of its initial density. Our demonstration that genomes can evolve through acquisition of addiction genes has implications for the general question of how a genome can evolve as a community of potentially selfish genes.

ONE of the impressive features of genomes, which became evident through decoding, is their fluidity within the evolutionary timescale. By fluidity, we mean acquisition of genes and genetic elements from outside the cell (horizontal transfer) ; internal genome rearrangements; or continuous loss, duplication, and allelic substitutions. The genomes are full of mobile, symbiotic, or parasitic genetic elements. Genome comparison and evolutionary analysis have revealed extensive horizontal transfer of genes between organisms, especially in bacterial and archaeal worlds (FAGUY and DOOLITTLE 2000). Rather than being a well-designed blueprint, a genome appears to be a temporary community of potentially mobile genes that essentially act selfishly. Given this feature of the genome, how are symbiosis and a cohesive social order, within a genome, ever achieved?

At the first glimpse inside the genomes, there are many genes, whose immediate advantage to the organism carrying them is unclear. An extreme and, therefore interesting, case is provided by the phenomenon of postsegregational killing or genetic addiction (KOBAYASHI 2004). In this phenomenon, the removal of a particular genetic element from the genome of an organism causes the product to induce death of the organism (Figure IA), although the organism lived normally before acquisition of this genetic element. An intact form of the genetic element would survive in other members of the host population.

As shown in Figure IB, a gene complex responsible for postsegregational killing (called an addiction gene complex here) consists of a set of closely linked genes that encodes a toxin and an antitoxin. The toxin's attack on a specific cellular target is blocked by the antitoxin at one of various steps. After loss of the gene complex (or some sort of disturbance in the balance between the two gene products), the antitoxin becomes ineffective, thereby permitting the toxin to attack its target.

Several type II restriction-modification systems (Figure 1C) have been experimentally proven to represent simple examples of postsegregational killing (??ιτ? et al. 1995). Here, the toxin is a restriction enzyme that attacks specific recognition sequences on the chromosome, while the antitoxin is a modification enzyme that protects these sequences by methylating them. The loss of the gene complex, followed by cell division, eventually dilutes the antitoxin level, causing the target sites on the newly replicated chromosomes to be exposed to lethal attack by the toxin (??ιτ? et al. 1995; KOBAYASHI 2004). In the second type of postsegregational killing system, called the classical proteic killer system or the toxin-antitoxin system, and labeled type A in Figure IB, the antitoxin counteracts the toxin action through direct interaction. …

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