Intragenomic conflict
From Biocrawler, the free encyclopedia.
The selfish gene theory postulates that natural selection will increase the frequency of those genes whose phenotypic effects ensure their sucessful replication. Generally, a gene achieve this goal by building in cooperation with other genes an organism capable of transmiting him to descendents. Intragenomic conflict arises when genes inside a genome are not transmited by the same rules, or when a gene causes its own transmission in detriment to the rest of the genome (this last kind of gene is usually called selfish genetic elements, or ultraselfish genes).
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Nuclear genes
This section deals with conflict between nuclear genes.
Meiotic drive
All nuclear genes in a given diploid genome cooperates because each allele have an equal probability of being present in a gamete. This fairness is guaranteed by the meiosis. But there is one type of gene, called segregation distorter, that cheat during meiosis or gametogenesis and thus are present in more than a half of the functional gametes. The most studied examples are sd in Drosophila melanogaster (fruit fly), t haplotype in Mus musculus (mouse) and sk in Neurospora sp. (fungus). Segregation distorters that are present in sexual chromosomes (as the Y chromosome in humans) are denominated sex-ratio distorters.
Maternal-effect lethals
The Medea gene causes the death of progeny from a heterozygous mother that do not inherit him. It occurs in the flour beetle (Tribolium castaneum)
Transposons
Transposons are autonomous replicating genes that encode the ability to move to new positions in the genome and therefore accumulate in the genomes. They replicate themselves in spite of being detrimental to the rest of the genome.
Homing endonuclease genes
Homing endonuclease genes (HEG) converts its rival allele into a copy of itself, thus being inherited in nearly all meiotic products of heterozygotes. They achieve this by encoding an endonuclease that breaks the rival allele. This break is repaired by using the sequence of the HEG as template.
Cytoplasmic genes
This section deals with conflict between nuclear and cytoplasmic genes.
Males as dead-ends to cytoplasmic genes
Anisogamy generally produces zygotes that inherits cytoplasmic elements exclusively from the feminine gamete. Thus, males represent dead-ends to these genes. Because of this fact, cytoplasmic genes have evolved a number of mechanisms that increase the production of female descendents and/or eliminates offspring not containing them.
Feminization
Organisms are converted into females by cytoplasmic inherited bacteria (Microsporidia and Wolbachia), regardless of nuclear sex-determing factors. It occurs in amphipod and isopod Crustacea and Lepidoptera.
Male-killing
Male embryos (in the case of cytoplasmic inherited bacteria) or male larvae (in the case of Microsporidia) are killed. It occurs in many insects.
Male-sterility
Anther tissue (male gametophyte) is killed by mitochondria in monoicous angiosperms, increasing energy and material spent in developing female gametophytes.
Parthenogenesis induction
Assexually produced males have chromosome complement doubled by Wolbachia, converting them into females. It occurs in haplodiploid Hymenoptera.
Cytoplasmic incompatibility
Zygotes produced by sperm of infected males and ova of non-infected females are killed by Wolbachia. It occurs in many arthropods.
References
- Dawkins, R. (1976) The selfish gene. Oxford University Press, Oxford. ISBN 0192177737
- Cosmides, L.M. & Tooby, J. (1981) Cytoplasmic inheritance and intragenomic conflict. Journal of Theoretical Biology, 89, 83-129.
- Hurst, L.D., Atlan A. & Bengtsson, B. O. (1996) Genetic conflicts. Quarterly Review of Biology, 71(3), 317-364.
- Hurst, G.D.D. & Werren J.H. (2001) The role of selsfish genetic elements in eukaryotic evolution. Nature Review Genetics, 2, 597-606.
- Burt, A. & Trivers, R.L. (2006) Genes in Conflict : The Biology of Selfish Genetic Elements. Belknap Press, Harvard. ISBN 0674017137
