Editing Selfish genetic element (section)

== Examples ==

=== Segregation distorters ===
[[File:Segregation distorters.png|thumb|Segregation distorters (here shown in red) get transmitted to >50% of the gametes.]]
Some selfish genetic elements manipulate the [[W:Transmission (genetics)|genetic transmission process]]  to their own advantage, and so end up being overrepresented in the gametes. Such distortion can occur in various ways, and the umbrella term that encompasses all of them is segregation distortion. Some elements can preferentially be transmitted in egg cells as opposed to [[polar body|polar bodies]] during meiosis, where only the former will be fertilized and transmitted to the next generation. Any gene that can manipulate the odds of ending up in the egg rather than the polar body will have a transmission advantage, and will increase in frequency in a population.<ref name=":21" />

Segregation distortion can happen in several ways. When this process occurs during meiosis it is referred to as [[W:meiotic drive|meiotic drive]]. Many forms of segregation distortion occur in male gamete formation, where there is differential mortality of spermatids during the process of sperm maturation or [[W:Spermiogenesis|spermiogenesis]]. The segregation distorter (SD) in ''Drosophila melanogaster'' is the best studied example, and it involves a nuclear envelope protein Ran-GAP and the X-linked repeat array called Responder (Rsp), where the SD allele of Ran-GAP favors its own transmission only in the presence of a Rsp<sup>sensitive</sup> allele on the homologous chromosome.<ref>{{cite journal | vauthors = Brittnacher JG, Ganetzky B | title = On the components of segregation distortion in Drosophila melanogaster. III. Nature of enhancer of SD | journal = Genetics | volume = 107 | issue = 3 | pages = 423–34 | date = July 1984 | doi = 10.1093/genetics/107.3.423 | pmid = 6428976 | pmc = 1202333 }}</ref><ref name=":26">{{cite journal | vauthors = Brittnacher JG, Ganetzky B | title = On the Components of Segregation Distortion in Drosophila melanogaster. II. Deletion Mapping and Dosage Analysis of the SD Locus | journal = Genetics | volume = 103 | issue = 4 | pages = 659–73 | date = April 1983 | doi = 10.1093/genetics/103.4.659 | pmid = 17246120 | pmc = 1202047 }}</ref><ref>{{cite journal | vauthors = Brittnacher JG, Ganetzky B | title = On the components of segregation distortion in Drosophila melanogaster. IV. Construction and analysis of free duplications for the Responder locus | journal = Genetics | volume = 121 | issue = 4 | pages = 739–50 | date = April 1989 | doi = 10.1093/genetics/121.4.739 | pmid = 2498160 | pmc = 1203657 }}</ref><ref>{{cite journal | vauthors = Powers PA, Ganetzky B | title = On the components of segregation distortion in Drosophila melanogaster. V. Molecular analysis of the Sd locus | journal = Genetics | volume = 129 | issue = 1 | pages = 133–44 | date = September 1991 | doi = 10.1093/genetics/129.1.133 | pmid = 1936954 | pmc = 1204561 }}</ref><ref>{{cite journal | vauthors = Larracuente AM, Presgraves DC | title = The selfish Segregation Distorter gene complex of Drosophila melanogaster | journal = Genetics | volume = 192 | issue = 1 | pages = 33–53 | date = September 2012 | pmid = 22964836 | pmc = 3430544 | doi = 10.1534/genetics.112.141390 }}</ref> SD acts to kill RSP<sup>sensitive</sup> sperm, in a post-meiotic process (hence it is not strictly speaking meiotic drive). Systems like this can have interesting rock-paper-scissors dynamics, oscillating between the SD-RSP<sup>insensitive</sup>, SD+-RSP<sup>insensitive</sup> and SD+-RSP<sup>sensitive</sup> haplotypes. The SD-RSP<sup>sensitive</sup> haplotype is not seen because it essentially commits suicide.<ref name=":26" />

When segregation distortion acts on sex chromosomes, they can skew the sex ratio. The SR system in ''Drosophila pseudoobscura'', for example, is on the X chromosome, and XSR/Y males produce only daughters, whereas females undergo normal meiosis with Mendelian proportions of gametes.<ref name=":11">{{cite journal | vauthors = Curtsinger JW, Feldman MW | title = Experimental and Theoretical Analysis of the "Sex-Ratio" Polymorphism in Drosophila pseudoobscura | journal = Genetics | volume = 94 | issue = 2 | pages = 445–66 | date = February 1980 | doi = 10.1093/genetics/94.2.445 | pmid = 17249004 | pmc = 1214151 }}</ref><ref>{{cite journal | vauthors = Curtsinger JW | title = Artificial selection on the sex ratio in Drosophila pseudoobscura | journal = Journal of Heredity | date = 1981 | volume = 72 | issue = 6 | pages = 377–381 | doi = 10.1093/oxfordjournals.jhered.a109535 }}</ref> Segregation distortion systems would drive the favored allele to fixation, except that most of the cases where these systems have been identified have the driven allele opposed by some other selective force. One example is the lethality of the t-haplotype in mice,<ref name=":14">{{cite journal | vauthors = Lyon MF | title = Transmission ratio distortion in mice | journal = Annual Review of Genetics | volume = 37 | pages = 393–408 | date = 2003 | pmid = 14616067 | doi = 10.1146/annurev.genet.37.110801.143030 }}</ref> another is the effect on male fertility of the Sex Ratio system in ''D. pseudoobscura''.<ref name=":11" />

=== Homing endonucleases ===
[[File:Homing endonucleases.png|thumb|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.]]
A phenomenon closely related to segregation distortion is [[homing endonuclease]]s.<ref name=":15">{{cite journal | vauthors = Burt A | title = Site-specific selfish genes as tools for the control and genetic engineering of natural populations | journal = Proceedings. Biological Sciences | volume = 270 | issue = 1518 | pages = 921–8 | date = May 2003 | pmid = 12803906 | pmc = 1691325 | doi = 10.1098/rspb.2002.2319 }}</ref><ref>{{cite journal | vauthors = Burt A, Koufopanou V | title = Homing endonuclease genes: the rise and fall and rise again of a selfish element | journal = Current Opinion in Genetics & Development | volume = 14 | issue = 6 | pages = 609–15 | date = December 2004 | pmid = 15531154 | doi = 10.1016/j.gde.2004.09.010 }}</ref><ref>{{cite journal | vauthors = Windbichler N, Menichelli M, Papathanos PA, Thyme SB, Li H, Ulge UY, Hovde BT, Baker D, Monnat RJ, Burt A, Crisanti A | title = A synthetic homing endonuclease-based gene drive system in the human malaria mosquito | journal = Nature | volume = 473 | issue = 7346 | pages = 212–5 | date = May 2011 | pmid = 21508956 | pmc = 3093433 | doi = 10.1038/nature09937 | bibcode = 2011Natur.473..212W }}</ref> These are enzymes that cut DNA in a sequence-specific way, and those cuts, generally double-strand breaks, are then "healed" by the regular DNA repair machinery. Homing endonucleases insert themselves into the genome at the site homologous to the first insertion site, resulting in a conversion of a heterozygote into a homozygote bearing a copy of the homing endonuclease on both homologous chromosomes. This gives homing endonucleases an allele frequency dynamics rather similar to a segregation distortion system, and generally unless opposed by strong countervailing selection, they are expected to go to fixation in a population. [[CRISPR|CRISPR-Cas9]] technology allows the artificial construction of homing endonuclease systems. These so-called "gene drive" systems pose a combination of great promise for biocontrol but also potential risk.<ref name=":16">Gantz VM, Bier E. Genome editing. The mutagenic chain reaction: a method for converting heterozygous to homozygous mutations. Science. 2015;348: 442–444.</ref><ref name=":17">{{cite journal | vauthors = Esvelt KM, Smidler AL, Catteruccia F, Church GM | title = Concerning RNA-guided gene drives for the alteration of wild populations | journal = eLife | volume = 3 | date = July 2014 | pmid = 25035423 | pmc = 4117217 | doi = 10.7554/eLife.03401 | doi-access = free }}</ref>

=== Transposable elements ===
[[File:Transposable elements (2).png|thumb|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).]]
Transposable elements (TEs) include a wide variety of DNA sequences that all have the ability to move to new locations in the genome of their host. Transposons do this by a direct cut-and-paste mechanism, whereas retrotransposons need to produce an RNA intermediate to move. TEs were first discovered in maize by [[Barbara McClintock]] in the 1940s<ref name=":8" /> and their ability to occur in both active and quiescent states in the genome was also first elucidated by McClintock.<ref>{{cite journal | vauthors = Ravindran S | title = Barbara McClintock and the discovery of jumping genes | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 50 | pages = 20198–9 | date = December 2012 | pmid = 23236127 | pmc = 3528533 | doi = 10.1073/pnas.1219372109 | doi-access = free }}</ref> TEs have been referred to as selfish genetic elements because they have some control over their own propagation in the genome. Most random insertions into the genome appear to be relatively innocuous, but they can disrupt critical gene functions with devastating results.<ref>Lisch D. How important are transposons for plant evolution? Nat Rev Genet. 2013;14: 49–61.</ref> For example, TEs have been linked to a variety of human diseases, ranging from cancer to haemophilia.<ref name=":29">{{cite journal | vauthors = Hancks DC, Kazazian HH | title = Roles for retrotransposon insertions in human disease | journal = Mobile DNA | volume = 7 | pages = 9 | date = 2016 | pmid = 27158268 | pmc = 4859970 | doi = 10.1186/s13100-016-0065-9 | doi-access = free }}</ref> TEs that tend to avoid disrupting vital functions in the genome tend to remain in the genome longer, and hence they are more likely to be found in innocuous locations.<ref name=":29" />

Both plant and animal hosts have evolved means for reducing the fitness impact of TEs, both by directly silencing them and by reducing their ability to transpose in the genome. It would appear that hosts in general are fairly tolerant of TEs in their genomes, since a sizable portion (30-80%) of the genome of many animals and plants is TEs.<ref name=":18">{{cite journal | vauthors = Ågren JA, Wright SI | title = Co-evolution between transposable elements and their hosts: a major factor in genome size evolution? | journal = Chromosome Research  | volume = 19 | issue = 6 | pages = 777–86 | date = August 2011 | pmid = 21850458 | doi = 10.1007/s10577-011-9229-0 | s2cid = 25148109 }}</ref><ref name=":19">T{{cite journal | vauthors = Tenaillon MI, Hollister JD, Gaut BS | title = A triptych of the evolution of plant transposable elements | journal = Trends in Plant Science | volume = 15 | issue = 8 | pages = 471–8 | date = August 2010 | pmid = 20541961 | doi = 10.1016/j.tplants.2010.05.003 }}</ref> When the host is able to stop their movement, TEs can simply be frozen in place, and it then can take millions of years for them to mutate away. The fitness of a TE is a combination of its ability to expand in numbers within a genome, to evade host defenses, but also to avoid eroding host fitness too drastically. The effect of TEs in the genome is not entirely selfish. Because their insertion into the genome can disrupt gene function, sometimes those disruptions can have positive fitness value for the host. Many adaptive changes in ''Drosophila''<ref>{{cite journal | vauthors = Aminetzach YT, Macpherson JM, Petrov DA | title = Pesticide resistance via transposition-mediated adaptive gene truncation in Drosophila | journal = Science | volume = 309 | issue = 5735 | pages = 764–7 | date = July 2005 | pmid = 16051794 | doi = 10.1126/science.1112699 | bibcode = 2005Sci...309..764A | s2cid = 11640993 }}</ref> and dogs<ref>{{cite journal | vauthors = Cordaux R, Batzer MA | title = Teaching an old dog new tricks: SINEs of canine genomic diversity | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 5 | pages = 1157–8 | date = January 2006 | pmid = 16432182 | pmc = 1360598 | doi = 10.1073/pnas.0510714103 | bibcode = 2006PNAS..103.1157C | doi-access = free }}</ref> for example, are associated with TE insertions.

=== B chromosomes ===
[[B chromosome]]s refer to chromosomes that are not required for the viability or fertility of the organism, but exist in addition to the normal (A) set.<ref>{{cite book | vauthors = Douglas RN, Birchler JA | veditors = Bhat T, Wani A | chapter = B Chromosomes | title = Chromosome Structure and Aberrations | publisher = Springer | location = New Delhi | date = 2017 | pages = 13–39 | doi = 10.1007/978-81-322-3673-3_2 | isbn = 978-81-322-3673-3 }}</ref> They persist in the population and accumulate because they have the ability to propagate their own transmission independently of the A chromosomes. They often vary in copy number between individuals of the same species.

B chromosomes were first detected over a century ago.{{When|date=December 2021}}<ref>{{cite journal | vauthors = Wilson E | title = The supernumerary chromosomes of Hemiptera. | journal = Science | date = 1907 | volume = 26 | pages = 870–871 }}</ref> Though typically smaller than normal chromosomes, their gene poor, heterochromatin-rich structure made them visible to early cytogenetic techniques. B chromosomes have been thoroughly studied and are estimated to occur in 15% of all eukaryotic species.<ref>{{cite journal | vauthors = Beukeboom LW | title = Bewildering Bs: an impression of the first B-Chromosome Conference. | journal = Heredity | year = 1994 | volume = 73 | issue = 3 | pages = 328–336 | doi = 10.1038/hdy.1994.140 | doi-access = free }}</ref> In general, they appear to be particularly common among eudicot plants, rare in mammals, and absent in birds. In 1945, they were the subject of Gunnar Östergren's classic paper "Parasitic nature of extra fragment chromosomes", where he argues that the variation in abundance of B chromosomes between and within species is because of the parasitic properties of the Bs.<ref name=":6" /> This was the first time genetic material was referred to as "parasitic" or "selfish". B chromosome number correlates positively with genome size<ref name=":12">{{cite journal | vauthors = Trivers R, Burt A, Palestis BG | title = B chromosomes and genome size in flowering plants | journal = Genome | volume = 47 | issue = 1 | pages = 1–8 | date = February 2004 | pmid = 15060596 | doi = 10.1139/g03-088 }}</ref> and has also been linked to a decrease in egg production in the grasshopper ''Eyprepocnemis plorans''.<ref>{{cite journal | vauthors = Zurita S, Cabrero J, López-León MD, Camacho JP | title = Polymorphism regeneration for a neutralized selfish B chromosome | journal = Evolution; International Journal of Organic Evolution | volume = 52 | issue = 1 | pages = 274–277 | date = February 1998 | pmid = 28568137 | doi = 10.1111/j.1558-5646.1998.tb05163.x | s2cid = 2588754 }}.</ref>

[[File:Cell with transmission patterns.png|thumb|Genetic conflicts often arise because not all genes are inherited in the same way. Examples include cytoplasmic male sterility (see [[#Selfish mitochondria|Selfish mitochondria]]). While mitochondrial and chloroplast genes are generally maternally inherited, B chromosomes can be preferentially transmitted through both males and females.]]

=== Selfish mitochondria ===
Genomic conflicts often arise because not all genes are inherited in the same way. Probably the best example of this is the conflict between [[Uniparental inheritance|uniparentally]] (usually but not always, maternally) inherited mitochondrial and biparentally inherited nuclear genes. Indeed, one of the earliest clear statements about the possibility of genomic conflict was made by the English botanist Dan Lewis in reference to the conflict between maternally inherited mitochondrial and biparentally inherited nuclear genes over sex allocation in [[Hermaphrodite|hermaphroditic]] plants.<ref name=":7" />

A single cell typically contains multiple mitochondria, creating a situation for competition over transmission. Uniparental inheritance has been suggested to be a way to reduce the opportunity for selfish mitochondria to spread, as it ensures all mitochondria share the same genome, thus removing the opportunity for competition.<ref name=":20" /><ref>{{cite journal | vauthors = Hadjivasiliou Z, Lane N, Seymour RM, Pomiankowski A | title = Dynamics of mitochondrial inheritance in the evolution of binary mating types and two sexes | journal = Proceedings. Biological Sciences | volume = 280 | issue = 1769 | pages = 20131920 | date = October 2013 | pmid = 23986113 | pmc = 3768323 | doi = 10.1098/rspb.2013.1920 }}</ref><ref>{{cite journal | vauthors = Law R, Hutson V | title = Intracellular symbionts and the evolution of uniparental cytoplasmic inheritance | journal = Proceedings. Biological Sciences | volume = 248 | issue = 1321 | pages = 69–77 | date = April 1992 | pmid = 1355912 | doi = 10.1098/rspb.1992.0044 | bibcode = 1992RSPSB.248...69L | s2cid = 45755461 }}</ref> This view remains widely held, but has been challenged.<ref>{{cite journal | vauthors = Christie JR, Schaerf TM, Beekman M | title = Selection against heteroplasmy explains the evolution of uniparental inheritance of mitochondria | journal = PLOS Genetics | volume = 11 | issue = 4 | pages = e1005112 | date = April 2015 | pmid = 25880558 | pmc = 4400020 | doi = 10.1371/journal.pgen.1005112 | doi-access = free }}</ref> Why inheritance ended up being maternal, rather than paternal, is also much debated, but one key hypothesis is that the mutation rate is lower in female compared to male gametes.<ref>{{cite journal | vauthors = Greiner S, Sobanski J, Bock R | title = Why are most organelle genomes transmitted maternally? | journal = BioEssays | volume = 37 | issue = 1 | pages = 80–94 | date = January 2015 | pmid = 25302405 | pmc = 4305268 | doi = 10.1002/bies.201400110 }}</ref>

The conflict between mitochondrial and nuclear genes is especially easy to study in flowering plants.<ref>{{cite journal | vauthors = Liu XQ, Xu X, Tan YP, Li SQ, Hu J, Huang JY, Yang DC, Li YS, Zhu YG | title = Inheritance and molecular mapping of two fertility-restoring loci for Honglian gametophytic cytoplasmic male sterility in rice (Oryza sativaL.) | journal = Molecular Genetics and Genomics | volume = 271 | issue = 5 | pages = 586–94 | date = June 2004 | pmid = 15057557 | doi = 10.1007/s00438-004-1005-9 | s2cid = 1898106 }}</ref><ref>{{cite journal | vauthors = Schnable PS, Wise RP | title = The molecular basis of cytoplasmic male sterility and fertility restoration. | journal = Trends Plant Sci. | date = 1998 | volume = 3 | issue = 5 | pages = 175–180 | doi = 10.1016/S1360-1385(98)01235-7 }}</ref> Flowering plants are typically hermaphrodites,<ref>Barrett SCH. The evolution of plant sexual diversity. Nat Rev Genet. 2002;3: 274–284.</ref> and the conflict thus occurs within a single individual. Mitochondrial genes are typically only transmitted through female gametes, and therefore from their point of view the production of pollen leads to an evolutionary dead end. Any mitochondrial mutation that can affect the amount of resources the plant invests in the female reproductive functions at the expense of the male reproductive functions improves its own chance of transmission. [[Cytoplasmic male sterility]] is the loss of male fertility, typically through loss of functional pollen production, resulting from a mitochondrial mutation.<ref>{{cite journal | vauthors = Hanson MR, Bentolila S | title = Interactions of mitochondrial and nuclear genes that affect male gametophyte development | journal = The Plant Cell | volume = 16 | issue = Suppl | pages = S154–69 | date = 2004 | pmid = 15131248 | pmc = 2643387 | doi = 10.1105/tpc.015966 }}</ref> In many species where cytoplasmic male sterility occurs, the nuclear genome has evolved so-called restorer genes, which repress the effects of the cytoplasmic male sterility genes and restore the male function, making the plant a hermaphrodite again.<ref>{{cite journal | vauthors = Budar F, Pelletier G | title = Male sterility in plants: occurrence, determinism, significance and use | journal = Comptes Rendus de l'Académie des Sciences, Série III | volume = 324 | issue = 6 | pages = 543–50 | date = June 2001 | pmid = 11455877 | doi = 10.1016/S0764-4469(01)01324-5}}</ref><ref>{{cite journal | vauthors = Budar F, Touzet P, De Paepe R | title = The nucleo-mitochondrial conflict in cytoplasmic male sterilities revisited | journal = Genetica | volume = 117 | issue = 1 | pages = 3–16 | date = January 2003 | pmid = 12656568 | doi = 10.1023/A:1022381016145 | s2cid = 20114356 }}</ref>

The co-evolutionary arms race between selfish mitochondrial genes and nuclear compensatory alleles can often be detected by crossing individuals from different species that have different combinations of male sterility genes and nuclear restorers, resulting in hybrids with a mismatch.<ref>{{cite journal | vauthors = Case AL, Finseth FR, Barr CM, Fishman L | title = Selfish evolution of cytonuclear hybrid incompatibility in Mimulus | journal = Proceedings. Biological Sciences | volume = 283 | issue = 1838 | pages = 20161493| date = September 2016 | pmid = 27629037 | pmc = 5031664 | doi = 10.1098/rspb.2016.1493 }}</ref>

Another consequence of the maternal inheritance of the mitochondrial genome is the so-called [[Mother's curse|Mother's Curse]].<ref>{{cite journal | vauthors = Gemmell NJ, Metcalf VJ, Allendorf FW | title = Mother's curse: the effect of mtDNA on individual fitness and population viability | journal = Trends in Ecology & Evolution | volume = 19 | issue = 5 | pages = 238–44 | date = May 2004 | pmid = 16701262 | doi = 10.1016/j.tree.2004.02.002 }}</ref> Because genes in the mitochondrial genome are strictly maternally inherited, mutations that are beneficial in females can spread in a population even if they are deleterious in males.<ref>{{cite journal | vauthors = Frank SA, Hurst LD | title = Mitochondria and male disease | journal = Nature | volume = 383 | issue = 6597 | pages = 224 | date = September 1996 | pmid = 8805695 | doi = 10.1038/383224a0 | bibcode = 1996Natur.383..224F | s2cid = 4337540 | doi-access = free }}</ref> Explicit screens in fruit flies have successfully identified such female-neutral but male-harming mtDNA mutations.<ref>{{cite journal | vauthors = Camus MF, Clancy DJ, Dowling DK | title = Mitochondria, maternal inheritance, and male aging | journal = Current Biology | volume = 22 | issue = 18 | pages = 1717–21 | date = September 2012 | pmid = 22863313 | doi = 10.1016/j.cub.2012.07.018 | doi-access = free | bibcode = 2012CBio...22.1717C }}</ref><ref>{{cite journal | vauthors = Patel MR, Miriyala GK, Littleton AJ, Yang H, Trinh K, Young JM, Kennedy SR, Yamashita YM, Pallanck LJ, Malik HS | title = A mitochondrial DNA hypomorph of cytochrome oxidase specifically impairs male fertility in Drosophila melanogaster | journal = eLife | volume = 5 | date = August 2016 | pmid = 27481326 | pmc = 4970871 | doi = 10.7554/eLife.16923 | doi-access = free }}</ref> Furthermore, a 2017 paper showed how a mitochondrial mutation causing [[Leber's hereditary optic neuropathy]], a male-biased eye disease, was brought over by one of the [[King's Daughters|''Filles du roi'']] that arrived in Quebec, Canada, in the 17th century and subsequently spread among many descendants.<ref>{{cite journal | vauthors = Milot E, Moreau C, Gagnon A, Cohen AA, Brais B, Labuda D | title = Mother's curse neutralizes natural selection against a human genetic disease over three centuries | journal = Nature Ecology & Evolution | volume = 1 | issue = 9 | pages = 1400–1406 | date = September 2017 | pmid = 29046555 | doi = 10.1038/s41559-017-0276-6 | bibcode = 2017NatEE...1.1400M | s2cid = 4183585 }}</ref>

=== Genomic imprinting ===
[[File:Imprt.png|thumb|''Igf2''&nbsp;is an example of genomic imprinting. In mice, the insulin-like growth factor 2 gene,&nbsp;''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&nbsp;''Igf2r'', which binds the growth protein and so slows growth, is maternally expressed (paternally silenced).&nbsp;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.<ref>{{cite journal | vauthors = Barlow DP, Bartolomei MS | title = Genomic imprinting in mammals | journal = Cold Spring Harbor Perspectives in Biology | volume = 6 | issue = 2 | pages = a018382 | date = February 2014 | pmid = 24492710 | pmc = 3941233 | doi = 10.1101/cshperspect.a018382 }}</ref>]]
Another sort of conflict that genomes face is that between the mother and father competing for control of gene expression in the offspring, including the complete silencing of one parental allele. Due to differences in methylation status of gametes, there is an inherent asymmetry to the maternal and paternal genomes that can be used to drive a differential parent-of-origin expression. This results in a violation of Mendel's rules at the level of expression, not transmission, but if the gene expression affects fitness, it can amount to a similar result.<ref name=":22" />

Imprinting seems like a maladaptive phenomenon, since it essentially means giving up diploidy, and heterozygotes for one defective allele are in trouble if the active allele is the one that is silenced. Several human diseases, such as [[Prader–Willi syndrome|Prader-Willi]] and [[Angelman syndrome|Angelman]] syndromes, are associated with defects in imprinted genes. The asymmetry of maternal and paternal expression suggests that some kind of conflict between these two genomes might be driving the evolution of imprinting. In particular, several genes in placental mammals display expression of paternal genes that maximize offspring growth, and maternal genes that tend to keep that growth in check. Many other conflict-based theories about the evolution of genomic imprinting have been put forward.<ref>{{cite journal | vauthors = Moore T, Haig D | title = Genomic imprinting in mammalian development: a parental tug-of-war | journal = Trends in Genetics | volume = 7 | issue = 2 | pages = 45–9 | date = February 1991 | pmid = 2035190 | doi = 10.1016/0168-9525(91)90230-N }}</ref><ref>{{cite journal | vauthors = Haig D | title = Coadaptation and conflict, misconception and muddle, in the evolution of genomic imprinting | journal = Heredity | volume = 113 | issue = 2 | pages = 96–103 | date = August 2014 | pmid = 24129605 | pmc = 4105449 | doi = 10.1038/hdy.2013.97 }}</ref>

At the same time, genomic or sexual conflict are not the only possible mechanisms whereby imprinting can evolve.<ref name=":22">{{cite journal | vauthors = Spencer HG, Clark AG | title = Non-conflict theories for the evolution of genomic imprinting | journal = Heredity | volume = 113 | issue = 2 | pages = 112–8 | date = August 2014 | pmid = 24398886 | pmc = 4105448 | doi = 10.1038/hdy.2013.129 }}</ref> Several molecular mechanisms for genomic imprinting have been described, and all have the aspect that maternally and paternally derived alleles are made to have distinct epigenetic marks, in particular the degree of methylation of cytosines. An important point to note regarding genomic imprinting is that it is quite heterogeneous, with different mechanisms and different consequences of having single parent-of-origin expression. For example, examining the imprinting status of closely related species allows one to see that a gene that is moved by an inversion into close proximity of imprinted genes may itself acquire an imprinted status, even if there is no particular fitness consequence of the imprinting.<ref name=":22" />

=== Greenbeards ===
A [[green-beard effect|greenbeard gene]] is a gene that has the ability to recognize copies of itself in other individuals and then make its carrier act preferentially toward such individuals. The name itself comes from thought-experiment first presented by William Hamilton<ref name=":27">{{cite journal | vauthors = Hamilton WD | title = The genetical evolution of social behaviour. I | journal = Journal of Theoretical Biology | volume = 7 | issue = 1 | pages = 1–16 | date = July 1964 | pmid = 5875341 | doi = 10.1016/0022-5193(64)90038-4| bibcode = 1964JThBi...7....1H | s2cid = 5310280 }}</ref> and then it was developed and given its current name by Richard Dawkins in ''The Selfish Gene.'' The point of the thought experiment was to highlight that from a gene's-eye view, it is not the genome-wide relatedness that matters (which is usually how kin selection operates, i.e. cooperative behavior is directed towards relatives), but the relatedness at the particular locus that underlies the social behavior.<ref name="TSG" /><ref name=":27" />

[[File:GreenbeardsAug18.png|thumb|The simplest form of greenbeard mechanism. An individual with the greenbeard allele preferentially helps a fellow greenbeard individual.]]

Following Dawkins, a greenbeard is usually defined as a gene, or set of closely linked genes, that has three effects:<ref>{{cite journal | vauthors = Gardner A, West SA | title = Greenbeards | journal = Evolution; International Journal of Organic Evolution | volume = 64 | issue = 1 | pages = 25–38 | date = January 2010 | pmid = 19780812 | doi = 10.1111/j.1558-5646.2009.00842.x | s2cid = 221733134 }}</ref>

# It gives carriers of the gene a phenotypic label, such as a greenbeard.
# The carrier is able to recognize other individuals with the same label.
# The carrier then behaves altruistically towards individuals with the same label.

Greenbeards were long thought to be a fun theoretical idea, with limited possibility of them actually existing in nature. However, since its conception, several examples have been identified, including in yeast,<ref>{{cite journal | vauthors = Smukalla S, Caldara M, Pochet N, Beauvais A, Guadagnini S, Yan C, Vinces MD, Jansen A, Prevost MC, Latgé JP, Fink GR, Foster KR, Verstrepen KJ | display-authors = 6 | title = FLO1 is a variable green beard gene that drives biofilm-like cooperation in budding yeast | journal = Cell | volume = 135 | issue = 4 | pages = 726–37 | date = November 2008 | pmid = 19013280 | pmc = 2703716 | doi = 10.1016/j.cell.2008.09.037 }}</ref> slime moulds,<ref>{{cite journal | vauthors = Queller DC, Ponte E, Bozzaro S, Strassmann JE | title = Single-gene greenbeard effects in the social amoeba Dictyostelium discoideum | journal = Science | volume = 299 | issue = 5603 | pages = 105–6 | date = January 2003 | pmid = 12511650 | doi = 10.1126/science.1077742 | bibcode = 2003Sci...299..105Q | s2cid = 30039249 }}</ref> and fire ants.<ref>{{cite journal | vauthors = Keller L, Ross KG | title = Selfish genes: a green beard in the red fire ant. | journal = Nature | year = 1998 | volume = 394 | issue = 6693 | pages = 573–575 | doi = 10.1038/29064 | bibcode = 1998Natur.394..573K | s2cid = 4310467 }}</ref> &nbsp;

There has been some debate whether greenbeard genes should be considered selfish genetic elements.<ref>{{cite journal | vauthors = Ridley M, Grafen A | title = Are green beard genes outlaws? | journal = Anim. Behav. | date = 1981 | volume = 29 | issue = 3 | pages = 954–955 | doi = 10.1016/S0003-3472(81)80034-6 | s2cid = 53167671 }}</ref><ref>{{cite journal | vauthors = Alexander RD, Bargia G | title = Group Selection, Altruism, and the Levels of Organization of Life. | journal = Annu Rev Ecol Syst | date = 1978 | volume = 9 | pages = 449–474 | doi = 10.1146/annurev.es.09.110178.002313 }}</ref><ref name=":23">{{cite journal | vauthors = Biernaskie JM, West SA, Gardner A | title = Are greenbeards intragenomic outlaws? | journal = Evolution; International Journal of Organic Evolution | volume = 65 | issue = 10 | pages = 2729–42 | date = October 2011 | pmid = 21967416 | doi = 10.1111/j.1558-5646.2011.01355.x | s2cid = 6958192 }}</ref> Conflict between a greenbeard locus and the rest of the genome can arise because during a given social interaction between two individuals, the relatedness at the greenbeard locus can be higher than at other loci in the genome. As a consequence, it may in the interest of the greenbeard locus to perform a costly social act, but not in the interest of the rest of the genome.<ref name=":23" />

In conjunction with selfish genetic elements, greenbeard selection has also been used as a theoretical explanation for suicide.<ref>{{Cite journal|last=Wiley|first=James C.|date=2020-12-01|title=Psychological Aposematism: An Evolutionary Analysis of Suicide|journal=Biological Theory|language=en|volume=15|issue=4|pages=226–238|doi=10.1007/s13752-020-00353-8|s2cid=219734814|issn=1555-5550|doi-access=free}}</ref>