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Corrected language issues in the overview, added a section on modifier genes
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'''Oligogenic inheritance''' ([[Ancient Greek|Greek]] ὀλίγος – ''ὀligos'' = few, a little) is a concept introduced after it was learned that the model of inheritance of most of the previously described "monogenic traits" cannot validly explain the [[phenotype]] distribution in the offspring of certain types of reproductive couples. It may be noted that the exposed theory concept of monogenic control of the [[phenotypic]] traits based on the classic route: one [[gene]] – one feature. There is a small number of genes involved in the control of only one property, and it seems that even fewer features that are controlled by the alleles from only one [[locus (genetics)|locus]].
'''Oligogenic inheritance''' ([[Ancient Greek|Greek]] ὀλίγος – ''ὀligos'' = few, a little) describes a trait that is influenced by more than one gene. Oligogenic inheritance represents an intermediate between [[monogenic inheritance]] in which a trait is determined by a single causative gene, and [[polygenic inheritance]], in which a trait is influenced by many genes and often environmental factors.<ref name=Badano2002>{{cite journal|last1=Badano|first1=Jose L.|last2=Katsanis|first2=Nicholas|title=Beyond Mendel: an evolving view of human genetic disease transmission|journal=Nature Reviews Genetics|date=October 2002|volume=3|issue=10|pages=779–789|doi=10.1038/nrg910}}</ref>


Historically, many traits were anticipated to be able to be linked to a single causative gene (in what is deemed [[monogenic inheritance]]), however work in genetics revealed that these traits are comparatively rare, and in most cases so-called monogenic traits are predominantly influenced by one gene, but can be mediated by other genes of small effect.<ref>{{cite journal|last1=Robinson|first1=Jon F.|last2=Katsanis|first2=Nicholas|title=Oligogenic Disease|journal=Vogel and Motulsky's Human Genetics|date=2010|pages=243–262|doi=10.1007/978-3-540-37654-5_8|url=https://doi.org/10.1007/978-3-540-37654-5_8|publisher=Springer, Berlin, Heidelberg|language=en}}</ref>
Although the modern [[genetics]] does not know the genes that control the absolutely only one [[phenotypic]] trait (but, logically, not one that is determined by a single gene!), the corresponding literature will (probably) long many traits treated as monogenic.<ref name=<“riger“>{{cite book|authors=Rieger R. Michaelis A., Green M. M.|year=1976|title=Glossary of genetics and cytogenetics: Classical and molecular|publisher=Springer-Verlag|place=Heidelberg – New York|isbn= 3-540-07668-9}}</ref><ref name=<“Hadzip“>{{cite book |author=Hadžiselimović R., Pojskić N. |year=2005|title= Uvod u humanu imunogenetiku.|publisher= Institut za genetičko inženjerstvo i biotehnologiju (INGEB), Sarajevo|isbn=9958-9344-3-4}}</ref><ref name=<“Hadzip“>{{cite book |author=Hadžiselimović R., Pojskić N. |year=2005|title= Uvod u humanu imunogenetiku.|publisher= Institut za genetičko inženjerstvo i biotehnologiju (INGEB), Sarajevo|isbn=9958-9344-3-4}}</ref><ref name=<“king“>{{cite book|authors=King R. C., Stransfield W. D.|year=1998|title=Dictionary of genetics|publisher=Oxford University Press|place= New York, Oxford|isbn=0-19-50944-1-7}}</ref>


==History==
Further studies, however, have shown that this simplification enough arguments to justify the prevailing view that the majority of ''monogenic'' features have '''oligogenic determination''', or that such traits genetically certain small number of '''oligogenes'''<ref>Rieger R. Michaelis A., Green M. M. (1976): Glossary of genetics and cytogenetics: Classical and molecular. Springer-Verlag, Heidelberg - New York, {{ISBN|3-540-07668-9}}; {{ISBN|0-387-07668-9}}.</ref><ref>Lawrence E. (1999): Henderson's Dictionary of biological terms. Longman Group Ltd., London, {{ISBN|0-582-22708-9}}.</ref> with a very dominant [[phenotypic]] effect ''[[major gene]]''; effect of other, so-called ''[[minor gene]]s'' from the corresponding [[oligogenic]] series (as well as environmental factors) on the expression of the observed characteristics is, in fact, practically negligible. It should be noted, however, that the difference between major and minor genes, as well as criteria for separating the oligogenic and [[polygene]]tically feature is still arbitrary.
⚫
The term oligogene was introduced by Keneth Mather (1941).<ref>Mather K. (1941): Variation and selection of polygenetic characters. J. Genet., 41: 159.</ref>


==Modifier genes==
⚫
The term oligogene into the science of inheritance was introduced by Keneth Mather (1941).<ref>Mather K. (1941): Variation and selection of polygenetic characters. J. Genet., 41: 159.</ref>
One example of oligogenic inheritance is a case where one gene will be the main causative factor behind a trait, however its [[penetrance]] or [[expressivity]] is influenced by another gene, called a modifier. This concept was recognised a long time ago,<ref>{{cite journal|last1=Haldane|first1=J. B. S.|title=The relative importance of principal and modifying genes in determining some human diseases|journal=Journal of Genetics|date=January 1941|volume=41|issue=2-3|pages=149–157|doi=10.1007/BF02983018}}</ref> however modern genetics techniques have improved our ability to detect cases of this phenomenon, revealing it to be more common that previously anticipated.<ref name=Badano2002></ref><ref>{{cite journal|last1=Dipple|first1=Katrina M.|last2=McCabe|first2=Edward R.B.|title=Phenotypes of Patients with “Simple” Mendelian Disorders Are Complex Traits: Thresholds, Modifiers, and Systems Dynamics|journal=The American Journal of Human Genetics|date=June 2000|volume=66|issue=6|pages=1729–1735|doi=10.1086/302938}}</ref>

==Identification of oligogenic traits==
A trait can be recognised as oligogenic through four lines of evidence:<ref name=Badano2002></ref>
*Phenotype–genotype correlations
*Phenotypic differences in an animal model of the disease that are dependent on the genetic background
*The identification of bona fide mutations that do not conform to monogenic inheritance
*The establishment of linkage to more than one locus or the failure to detect linkage using Mendelian models.


==Human properties with possible oligogenic inheritance==
==Human properties with possible oligogenic inheritance==
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== See also==
== See also==
*[[Gene]]
*[[Gene]]
*[[Feature]]{{dn|date=August 2017}}
*[[Monogenic inheritance]]
*[[Monogenic inheritance]]
*[[Polygenic inheritance]]
*[[Polygenic inheritance]]

Revision as of 16:04, 24 August 2017

Oligogenic inheritance (Greek ὀλίγος – ὀligos = few, a little) describes a trait that is influenced by more than one gene. Oligogenic inheritance represents an intermediate between monogenic inheritance in which a trait is determined by a single causative gene, and polygenic inheritance, in which a trait is influenced by many genes and often environmental factors.[1]

Historically, many traits were anticipated to be able to be linked to a single causative gene (in what is deemed monogenic inheritance), however work in genetics revealed that these traits are comparatively rare, and in most cases so-called monogenic traits are predominantly influenced by one gene, but can be mediated by other genes of small effect.[2]

History

The term oligogene was introduced by Keneth Mather (1941).[3]

Modifier genes

One example of oligogenic inheritance is a case where one gene will be the main causative factor behind a trait, however its penetrance or expressivity is influenced by another gene, called a modifier. This concept was recognised a long time ago,[4] however modern genetics techniques have improved our ability to detect cases of this phenomenon, revealing it to be more common that previously anticipated.[1][5]

Identification of oligogenic traits

A trait can be recognised as oligogenic through four lines of evidence:[1]

  • Phenotype–genotype correlations
  • Phenotypic differences in an animal model of the disease that are dependent on the genetic background
  • The identification of bona fide mutations that do not conform to monogenic inheritance
  • The establishment of linkage to more than one locus or the failure to detect linkage using Mendelian models.

Human properties with possible oligogenic inheritance

Dominant Recessive References
Widow's peak Straight frontal hair line [6][7]
Ocular hypertelorism Hypotelorism
Facial dimples * No facial dimples [8][9]
Able to taste PTC Unable to taste PTC [10]
Unattached (free) earlobe Attached earlobe [8][11][12]
Clockwise hair direction (left to right) Counter-clockwise hair direction (right to left) [13]
Cleft chin Smooth chin [14]
Ability to roll tongue (Able to hold tongue in a U shape) No ability to roll tongue [15]
Extra finger or toe Normal five fingers and toes [15]
Straight thumb Hitchhiker's thumb [15]
Freckles No freckles [8][16]
Wet-type earwax Dry-type earwax [11][17]
Shortness in fingers Normal finger length [15]
Webbed fingers Normal separated fingers [15]
Roman nose No prominent bridge [18]
Marfan's syndrome Normal body proportions [19]
Huntington's disease No nerve damage [20]
Normal mucus lining Cystic fibrosis [21]
Forged chin Receding chin [18]
White forelock Dark forelock [22]
Ligamentous angustus Ligamentous laxity [23]
Ability to eat sugar Galactosemia [24]
Total leukonychia and Bart pumphrey syndrome Partial leukonychia [25]
Absence of fish-like body odour Trimethylaminuria [26]
Lactose persistence * Lactose intolerance * [27]
Prominent chin (V-shaped) Less prominent chin (U-shaped) [28]

See also

References

  1. ^ a b c Badano, Jose L.; Katsanis, Nicholas (October 2002). "Beyond Mendel: an evolving view of human genetic disease transmission". Nature Reviews Genetics. 3 (10): 779–789. doi:10.1038/nrg910.
  2. ^ Robinson, Jon F.; Katsanis, Nicholas (2010). "Oligogenic Disease". Vogel and Motulsky's Human Genetics. Springer, Berlin, Heidelberg: 243–262. doi:10.1007/978-3-540-37654-5_8.
  3. ^ Mather K. (1941): Variation and selection of polygenetic characters. J. Genet., 41: 159.
  4. ^ Haldane, J. B. S. (January 1941). "The relative importance of principal and modifying genes in determining some human diseases". Journal of Genetics. 41 (2–3): 149–157. doi:10.1007/BF02983018.
  5. ^ Dipple, Katrina M.; McCabe, Edward R.B. (June 2000). "Phenotypes of Patients with "Simple" Mendelian Disorders Are Complex Traits: Thresholds, Modifiers, and Systems Dynamics". The American Journal of Human Genetics. 66 (6): 1729–1735. doi:10.1086/302938.
  6. ^ Campbell, Neil; Reece, Jane (2005). Biology. San Francisco: Benjamin Cummings. p. 265. ISBN 0-07-366175-9.
  7. ^ McKusick, Victor A. (10 February 2009). "Widow's Peak". Online Mendelian Inheritance in Man. Johns Hopkins University. 194000.
  8. ^ a b c "Genetics/Reproduction". ScienceNet – Life Science. Singapore Science Centre. Archived from the original on 2003-09-25. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  9. ^ McKusick, Victor A. (25 June 1994). "Dimples, Facial". Online Mendelian Inheritance in Man. Johns Hopkins University. 126100.
  10. ^ Wooding, Stephen (28 June 2004). "Natural selection at work in genetic variation to taste". Medial News Today. Archived from the original on 2007-12-13. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  11. ^ a b Cruz-Gonzalez, L.; Lisker, R. (1982). "Inheritance of ear wax types, ear lobe attachment and tongue rolling ability". Acta Anthropogenet. 6 (4): 247–54. PMID 7187238.
  12. ^ McKusick, Victor A.; Lopez, A (30 July 2010). "Earlobe Attachment, Attached vs. Unattached". Online Mendelian Inheritance in Man. Johns Hopkins University. 128900.
  13. ^ McDonald, John H. (8 December 2011). "Hair Whorl". Myths of Human Genetics. University of Delaware.
  14. ^ McKusick, Victor A. (23 March 2013). "Cleft Chin". Online Mendelian Inheritance in Man. Johns Hopkins University. 119000.
  15. ^ a b c d e Hadžiselimović R. (2005). Bioantropologija – Biodiverzitet recentnog čovjeka/Bioanthropology – Biodiversity of recent man. Sarajevo: INGEB. ISBN 9958-9344-2-6.
  16. ^ Xue-Jun Zhang; et al. (2004). "A Gene for Freckles Maps to Chromosome 4q32–q34". Journal of Investigative Dermatology. 122: 286–290. doi:10.1046/j.0022-202x.2004.22244.x.
  17. ^ McKusick, Victor A.; O'Neill, Marla J. F. (22 November 2010). "Apocrine Gland Secretion, Variation in". Online Mendelian Inheritance in Man. Johns Hopkins University. 117800.
  18. ^ a b "Mendelian Traits in Humans" (PDF). Human Genetics. San Diego Supercomputer Center (SDSC).
  19. ^ Chen, Harold. Buehler, Bruce (ed.). "Genetics of Marfan Syndrome". Medscape. WebMD LLC.
  20. ^ Stafford, Kate; Mannor, Michael. "Mutations and Genetic Disease". Genetic Diseases. ThinkQuest. Archived from the original on 2007-01-03. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  21. ^ "Autosomal Recessive: Cystic Fibrosis, Sickle Cell Anemia, Tay Sachs Disease". Medical Genetics. Children's Hospital of Pittsburgh. 3 February 2008. Archived from the original on 2009-08-24. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  22. ^ "Inherited Human Traits". EdQuest. Archived from the original on 2012-02-01. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  23. ^ Scott, C. I. (1971). "Unusual facies, joint hypermobility, genital anomaly and short stature: A new dysmorphic syndrome". Birth defects original article series. 7 (6): 240–246. PMID 5173168.
  24. ^ Fankhauser, D. B. (2 Feb 2006). "Human Heritable Traits". University of Cincinnati Clermont College.
  25. ^ Tüzün, Yalçın; Karaku, Özge (2009). "Leukonychia" (PDF). Journal of the Turkish Academy of Dermatology. JTAD.
  26. ^ "Learning About Trimethylaminuria". genome.gov. National Human Genome Research Institute.
  27. ^ Bowen, R. (25 April 2009). "Lactose Intolerance (Lactase Non-Persistence)". Colorado State University.
  28. ^ Jablecki, Donna Mae. "Variations on a Human Face" (PDF). Science Experiments on File. Facts on File.
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