Selfish DNA
Selfish DNA is a term for sequences of DNA that have two properties:
- the DNA sequence spreads by forming more copies of itself in the genome; and
- it does not help the reproductive success of its host organism. It may or may not have negative effects.
In his 1976 book, The Selfish Gene,[1] Richard Dawkins suggested the idea of selfish DNA when the noncoding DNA in eukaryotic genomes was discovered. In 1980, two articles in the journal Nature expanded and discussed the concept.[2][3] According to one of these articles:
The theory of natural selection, in its more general formulation, deals with the competition between replicating entities. It shows that, in such a competition, the more efficient replicators increase in number at the expense of their less efficient competitors. After a sufficient time, only the most efficient replicators survive.
– L.E. Orgel & F.H.C. Crick, Selfish DNA: the ultimate parasite.[3]
Normal genetically functional DNA might be seen as "replicating entities" that effect their replication by manipulating the cell that they control. In contrast, units of selfish DNA may exploit existing mechanisms in the cell, and multiply without affecting the fitness of the organism in other respects.
There is no sharp boundary between the concepts of selfish DNA and genetically functional DNA. Often it also is difficult to see if a unit of noncoding DNA is functionally important or not; or if important, in what way. What is more, it is not always easy to distinguish between some instances of selfish DNA and some types of viruses.
History of the idea
The idea that some genetic elements might not be useful to the organism is not a new one. In 1928, a Russian geneticist reported an X chromosome in Drosophila obscura.[4] He claimed that the resulting female-biased sex ratio might drive a population extinct.
In 1941 it was first suggested that there might be a conflict between normal inherited nuclear genes from both parents and mitochondrial genes from one parent (the female). It could lead to cytoplasmic male sterility in plants.[5]
Around the same time, several other examples of selfish genetic elements were reported. For example, a maize geneticist described how chromosomal knobs led to female meiotic drive in maize.[6] Meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time.
The Swedish botanist and cytogeneticist Gunnar Östergren in 1945 noted how chromosomes may spread in a population because of their own ”parasitic” nature.[7] Discussing B chromosomes in plants he wrote: ”In many cases these chromosomes have no useful function at all to the species carrying them, but that they often lead an exclusively parasitic existence … [B chromosomes] need not be useful for the plants. They need only be useful to themselves.” - Gunnar Östergren.[7]
Then, in the early 1950s, Barbara McClintock published a series of papers describing the existence of "transposable elements". These are among the most successful selfish genetic elements.[8] The discovery of transposable elements led to her being awarded the Nobel Prize in Medicine or Physiology in 1983.
Selfish DNA Media
Segregation distorters (here shown in red) get transmitted to >50% of the gametes.
Homing endonucleases can recognize a target sequence, cut it, and then use its own sequence as a template during double strand break repair. This converts a heterozygote into a homozygote.
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).
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.
The simplest form of greenbeard mechanism. An individual with the greenbeard allele preferentially helps a fellow greenbeard individual.
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References
- ↑ Dawkins, Richard R. (1976). The Selfish Gene. New York: Oxford University Press. ISBN 978-0-198-57519-1. OCLC 2681149.
- ↑ Doolittle W.F. & Sapienza C. (1980). "Selfish genes, the phenotype paradigm and genome evolution". Nature. 284 (5757): 601–603. Bibcode:1980Natur.284..601D. doi:10.1038/284601a0. PMID 6245369. S2CID 4311366.
- ↑ 3.0 3.1 Orgel L.E. & Crick F.H.C. (1980). "Selfish DNA: the ultimate parasite". Nature. 284 (5757): 604–607. Bibcode:1980Natur.284..604O. doi:10.1038/284604a0. PMID 7366731. S2CID 4233826.
- ↑ Gershenson S. (1928). "A new sex-ratio abnormality in Drosophila obscura". Genetics. 13 (6): 488–507. doi:10.1093/genetics/13.6.488. PMC 1200995. PMID 17246563.
- ↑ Lewis D. (1941). "Male sterility in natural populations of hermaphrodite plants the equilibrium between females and hermaphrodites to be expected with different types of inheritance". New Phytologist. 40 (1): 56–63. doi:10.1111/j.1469-8137.1941.tb07028.x.
- ↑ Rhoades M.M. (1942). "Preferential segregation in maize". Genetics. 27 (4): 395–407. doi:10.1093/genetics/27.4.395. PMC 1209167. PMID 17247049.
- ↑ 7.0 7.1 Östergren G (1945). "Parasitic nature of extra fragment chromosomes". Botaniska Notiser. 2: 157–163.
- ↑ McClintock B. (1950). "The origin and behavior of mutable loci in maize". Proceedings of the National Academy of Sciences of the United States of America. 36 (6): 344–55. Bibcode:1950PNAS...36..344M. doi:10.1073/pnas.36.6.344. PMC 1063197. PMID 15430309.