Editing Genomic imprinting (section)

===Hypotheses on the origins of imprinting===
A widely accepted hypothesis for the evolution of genomic imprinting is the "parental conflict hypothesis".<ref name="Moore and Haig 1991">{{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 = 45–49 | date = February 1991 | pmid = 2035190 | doi = 10.1016/0168-9525(91)90230-N }}</ref> Also known as the kinship theory of genomic imprinting, this hypothesis states that the inequality between parental genomes due to imprinting is a result of the [[sexual conflict|differing interests of each parent]] in terms of the [[fitness (biology)|evolutionary fitness of their genes]].<ref name="Haig 1997">{{cite journal | vauthors = Haig D | title = Parental antagonism, relatedness asymmetries, and genomic imprinting | journal = Proceedings. Biological Sciences | volume = 264 | issue = 1388 | pages = 1657–1662 | date = November 1997 | pmid = 9404029 | pmc = 1688715 | doi = 10.1098/rspb.1997.0230 | bibcode = 1997RSPSB.264.1657H | author-link = David Haig (biologist) }}</ref><ref name="Haig 2000">{{Cite journal |vauthors=Haig D |year=2000 |title=The kinship theory of genomic imprinting |journal=Annual Review of Ecology and Systematics |volume=31 |issue=1 |pages=9–32 |doi=10.1146/annurev.ecolsys.31.1.9|bibcode=2000AnRES..31....9H }}</ref> The [[father]]'s genes that encode for imprinting gain greater fitness through the success of the offspring, at the expense of the [[mother]]. The mother's evolutionary imperative is often to conserve resources for her own survival while providing sufficient nourishment to current and subsequent litters. Accordingly, paternally expressed genes tend to be growth-promoting whereas maternally expressed genes tend to be growth-limiting.<ref name="Moore and Haig 1991" /> In support of this hypothesis, genomic imprinting has been found in all placental mammals, where post-fertilisation offspring resource consumption at the expense of the mother is high; although it has also been found in [[oviparous]] birds<ref>{{cite journal | vauthors = McElroy JP, Kim JJ, Harry DE, Brown SR, Dekkers JC, Lamont SJ | title = Identification of trait loci affecting white meat percentage and other growth and carcass traits in commercial broiler chickens | journal = Poultry Science | volume = 85 | issue = 4 | pages = 593–605 | date = April 2006 | pmid = 16615342 | doi = 10.1093/ps/85.4.593 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Tuiskula-Haavisto M, Vilkki J | title = Parent-of-origin specific QTL--a possibility towards understanding reciprocal effects in chicken and the origin of imprinting | journal = Cytogenetic and Genome Research | volume = 117 | issue = 1–4 | pages = 305–312 | year = 2007 | pmid = 17675872 | doi = 10.1159/000103192 | s2cid = 27834663 }}</ref> where there is relatively little post-fertilisation resource transfer and therefore less parental conflict. A small number of imprinted genes are fast evolving under positive Darwinian selection possibly due to antagonistic co-evolution.<ref name="O'Connell_2010">{{cite journal | vauthors = O'Connell MJ, Loughran NB, Walsh TA, Donoghue MT, Schmid KJ, Spillane C | title = A phylogenetic approach to test for evidence of parental conflict or gene duplications associated with protein-encoding imprinted orthologous genes in placental mammals | journal = Mammalian Genome | volume = 21 | issue = 9–10 | pages = 486–498 | date = October 2010 | pmid = 20931201 | doi = 10.1007/s00335-010-9283-5 | s2cid = 6883377 }}</ref> The majority of imprinted genes display high levels of micro-[[synteny]] conservation and have undergone very few duplications in placental mammalian lineages.<ref name="O'Connell_2010" />

However, our understanding of the molecular mechanisms behind genomic imprinting show that it is the maternal genome that controls much of the imprinting of both its own and the paternally-derived genes in the zygote, making it difficult to explain why the maternal genes would willingly relinquish their dominance to that of the paternally-derived genes in light of the conflict hypothesis.<ref name="Keverne">{{cite journal | vauthors = Keverne EB, Curley JP | title = Epigenetics, brain evolution and behaviour | journal = Frontiers in Neuroendocrinology | volume = 29 | issue = 3 | pages = 398–412 | date = June 2008 | pmid = 18439660 | doi = 10.1016/j.yfrne.2008.03.001 | url = http://champagnelab.psych.columbia.edu/docs/frontiers.pdf | url-status = dead | access-date = 2011-01-06 | s2cid = 10697086 | archive-url = https://web.archive.org/web/20100622154417/http://champagnelab.psych.columbia.edu/docs/frontiers.pdf | archive-date = 2010-06-22 }}</ref>

Another hypothesis proposed is that some imprinted genes act coadaptively to improve both fetal development and maternal provisioning for nutrition and care.<ref name="Peters2014" /><ref name="Keverne" /><ref>{{cite journal | vauthors = Wolf JB | title = Cytonuclear interactions can favor the evolution of genomic imprinting | journal = Evolution; International Journal of Organic Evolution | volume = 63 | issue = 5 | pages = 1364–1371 | date = May 2009 | pmid = 19425202 | doi = 10.1111/j.1558-5646.2009.00632.x | s2cid = 29251471 }}</ref> In it, a subset of paternally expressed genes are co-expressed in both the placenta and the mother's hypothalamus. This would come about through selective pressure from parent-infant coadaptation to improve infant survival. Paternally expressed 3 (''[[PEG3]]'') is a gene for which this hypothesis may apply.<ref name="Peters2014" />

Others have approached their study of the origins of genomic imprinting from a different side, arguing that [[natural selection]] is operating on the role of epigenetic marks as machinery for homologous chromosome recognition during meiosis, rather than on their role in differential expression.<ref name="de Villena et al 2000">{{cite journal | vauthors = Pardo-Manuel de Villena F, de la Casa-Esperón E, Sapienza C | title = Natural selection and the function of genome imprinting: beyond the silenced minority | journal = Trends in Genetics | volume = 16 | issue = 12 | pages = 573–579 | date = December 2000 | pmid = 11102708 | doi = 10.1016/S0168-9525(00)02134-X }}</ref> This argument centers on the existence of epigenetic effects on chromosomes that do not directly affect gene expression, but do depend on which parent the chromosome originated from.<ref name="de la Casa-Esperon 2003">{{cite journal | vauthors = de la Casa-Esperón E, Sapienza C | title = Natural selection and the evolution of genome imprinting | journal = Annual Review of Genetics | volume = 37 | pages = 349–370 | year = 2003 | pmid = 14616065 | doi = 10.1146/annurev.genet.37.110801.143741 }}</ref> This group of epigenetic changes that depend on the chromosome's parent of origin (including both those that affect gene expression and those that do not) are called parental origin effects, and include phenomena such as paternal [[X inactivation]] in the [[marsupial]]s, nonrandom parental [[chromatid]] distribution in the ferns, and even mating type switching in yeast.<ref name="de la Casa-Esperon 2003" /> This diversity in organisms that show parental origin effects has prompted theorists to place the evolutionary origin of genomic imprinting before the last common ancestor of plants and animals, over a billion years ago.<ref name="de Villena et al 2000" />

Natural selection for genomic imprinting requires genetic variation in a population. A hypothesis for the origin of this genetic variation states that the host-defense system responsible for silencing foreign DNA elements, such as genes of viral origin, mistakenly silenced genes whose silencing turned out to be beneficial for the organism.<ref>{{cite journal | vauthors = Barlow DP | title = Methylation and imprinting: from host defense to gene regulation? | journal = Science | volume = 260 | issue = 5106 | pages = 309–310 | date = April 1993 | pmid = 8469984 | doi = 10.1126/science.8469984 | bibcode = 1993Sci...260..309B | s2cid = 6925971 }}</ref> There appears to be an over-representation of [[retrotransposon|retrotransposed genes]], that is to say genes that are inserted into the genome by [[virus]]es, among imprinted genes. It has also been postulated that if the retrotransposed gene is inserted close to another imprinted gene, it may just acquire this imprint.<ref name="Chai 2001">{{cite journal | vauthors = Chai JH, Locke DP, Ohta T, Greally JM, Nicholls RD | title = Retrotransposed genes such as Frat3 in the mouse Chromosome 7C Prader-Willi syndrome region acquire the imprinted status of their insertion site | journal = Mammalian Genome | volume = 12 | issue = 11 | pages = 813–821 | date = November 2001 | pmid = 11845283 | doi = 10.1007/s00335-001-2083-1 | s2cid = 13419814 }}</ref>