Editing Selfish genetic element (section)

=== 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" />