WordNet

of or relating to an inheritable character that is controlled by several genes at once; of or related to or determined by polygenes
involving or depending on several factors or causes (especially pertaining to a condition or disease resulting from the interaction of many genes)
a gene that by itself has little effect on the phenotype but which can act together with others to produce observable variations

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/02/02 17:19:01」(JST)

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A polygene, multiple factor, multiple gene inheritance, or quantitative gene is a group of non-allelic genes that together influence a phenotypic trait. The precise loci or identities of the non-allelic genes are often unknown to biologists. Advances in statistical methodology and high throughput sequencing are, however, allowing researchers to locate candidate genes for the trait. These genes are generally pleiotropic as well. The genes that contribute to type 2 diabetes are thought to be mostly polygenes.^[1]

Traits with polygenic determinism correspond to the classical quantitative characters, as opposed to the qualitative characters with monogenic or oligogenic determinism.

Inheritance

Polygenic inheritance occurs when one characteristic is controlled by two or more genes. Often the genes are large in quantity but small in effect.^[2] Examples of human polygenic inheritance are height, skin color and weight. Polygenes exist in other organisms, as well. Drosophila, for instance, display polygeny with traits such as wing morphology,^[3] bristle count^[4] and many others.

Trait distribution

The frequency of the phenotypes of these traits generally follows a normal continuous variation distribution pattern. This results from the many possible allelic combinations. When the values are plotted, a bell-shaped curve is obtained. The mode of the distribution represents the optimal, or fittest, phenotype. The more genes are involved, the smoother the estimated curve. However, in this model all genes must code for alleles with additive effects. This assumption is often unrealistic as many genes display epistasis effects which can have unpredictable effects on the distribution of outcomes, especially when looking at the distribution on a fine scale.^[5]

Mapping polygenes

Example of a genome-wide scan for QTL of osteoporosis

Traditionally, mapping polygenes requires statistical tools available to help measure the effects of polygenes as well as narrow in on single genes. One of these tools is QTL-mapping. QTL-mapping utilizes a phenomenon known as linkage disequilibrium by comparing known marker genes with correlated phenotypes. Often, researchers will find a large region of DNA, called a locus, that accounts for a significant amount of the variation observed in the measured trait. This locus will usually contain a large number of genes that are responsible. A new form of QTL has been described as expression QTL (eQTL). eQTLs regulate the amount of expressed mRNA, which in turn regulates the amount of protein within the organism.^[6]

Another interest of statistical geneticists using QTL mapping is to determine the complexity of the genetic architecture underlying a phenotypic trait. For example, they may be interested in knowing whether a phenotype is shaped by many independent loci, or by a few loci, and do those loci interact. This can provide information on how the phenotype may be evolving.

References

^ http://care.diabetesjournals.org/content/22/2/345.full.pdf+html
^ Falconer, D. S. & Mackay TFC (1996). Introduction to Quantitative Genetics. Fourth edition. Addison Wesley Longman, Harlow, Essex, UK.
^ http://www.genetics.org/cgi/reprint/155/2/671
^ http://service004.hpc.ncsu.edu/mackay/Good_Mackay_site/PUB_files/Mackay%202005%20Trends%20Genet.pdf
^ Ricki Lewis (2003), Multifactorial Traits, McGraw-Hill Higher Education, http://highered.mcgraw-hill.com/sites/007246268x/student_view0/chapter7/
^ Consoli L, Lefèvre A, Zivy M, de Vienne D, Damerval C (Apr 2002). "QTL analysis of proteome and transcriptome variations for dissecting the genetic architecture of complex traits in maize.". Plant Mol Biol. 48 (5-6): 575–581. doi:10.1023/A:1014840810203. PMID 11999835.

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English Journal

Genome-wide association uncovers shared genetic effects among personality traits and mood states.

Luciano M, Huffman JE, Arias-Vásquez A, Vinkhuyzen AA, Middeldorp CM, Giegling I, Payton A, Davies G, Zgaga L, Janzing J, Ke X, Galesloot T, Hartmann AM, Ollier W, Tenesa A, Hayward C, Verhagen M, Montgomery GW, Hottenga JJ, Konte B, Starr JM, Vitart V, Vos PE, Madden PA, Willemsen G, Konnerth H, Horan MA, Porteous DJ, Campbell H, Vermeulen SH, Heath AC, Wright A, Polasek O, Kovacevic SB, Hastie ND, Franke B, Boomsma DI, Martin NG, Rujescu D, Wilson JF, Buitelaar J, Pendleton N, Rudan I, Deary IJ.SourceCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK; Department of Psychology, University of Edinburgh, Edinburgh, UK. michelle.luciano@ed.ac.uk.
American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.Am J Med Genet B Neuropsychiatr Genet.2012 Sep;159B(6):684-95. doi: 10.1002/ajmg.b.32072. Epub 2012 May 24.
Measures of personality and psychological distress are correlated and exhibit genetic covariance. We conducted univariate genome-wide SNP (∼2.5 million) and gene-based association analyses of these traits and examined the overlap in results across traits, including a prediction analysis of mood st
PMID 22628180

Expression QTL analysis of top loci from GWAS meta-analysis highlights additional schizophrenia candidate genes.

de Jong S, van Eijk KR, Zeegers DW, Strengman E, Janson E, Veldink JH, van den Berg LH, Cahn W, Kahn RS, Boks MP, Ophoff RA; The PGC Schizophrenia (GWAS) Consortium.Source1] Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands [2] Department of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center, Utrecht, The Netherlands.
European journal of human genetics : EJHG.Eur J Hum Genet.2012 Sep;20(9):1004-1008. doi: 10.1038/ejhg.2012.38. Epub 2012 Mar 21.
There is genetic evidence that schizophrenia is a polygenic disorder with a large number of loci of small effect on disease susceptibility. Genome-wide association studies (GWASs) of schizophrenia have had limited success, with the best finding at the MHC locus at chromosome 6p. A recent effort of t
PMID 22433715

A genome-wide search for linkage to allergic rhinitis in Danish sib-pair families.

Kruse LV, Nyegaard M, Christensen U, Møller-Larsen S, Haagerup A, Deleuran M, Hansen LG, Venø SK, Goossens D, Del-Favero J, Børglum AD.Source1] Department of Biomedicine, Aarhus University, Aarhus, Denmark [2] Department of Paediatrics, Region Hospital Viborg, Viborg, Denmark.
European journal of human genetics : EJHG.Eur J Hum Genet.2012 Sep;20(9):965-72. doi: 10.1038/ejhg.2012.46. Epub 2012 Mar 14.
Allergic rhinitis (AR) is a complex disorder with a polygenic, multifactorial aetiology. Twin studies have found the genetic contribution to be substantial. We collected and clinically characterised a sample consisting of 127 Danish nuclear families with at least two siblings suffering from AR or al
PMID 22419170

Japanese Journal

ACE I/D, ACTN3 R577X, PPARD T294C and PPARGC1A Gly482Ser polymorphisms and physical fitness in Taiwanese late adolescent girls

CHIU Li-Ling,CHEN Tzu-Wen,HSIEH Sandy S.,HSIEH Ling-Ling
The journal of physiological sciences : JPS 62(2), 115-121, 2012-03-01
NAID 10030351633

Possible Involvement of Hypothalamic Nucleobindin-2 in Hyperphagic Feeding in Tsumura Suzuki Obese Diabetes Mice

Miyata Shigeo,Yamada Nao,Kawada Tomie
Biological and Pharmaceutical Bulletin 35(10), 1784-1793, 2012
… The aim of this study was to clarify the hypothalamic neuropeptides that are associated with hyperphagic feeding in Tsumura Suzuki Obese Diabetes (TSOD) mice, a model of type 2 diabetes with polygenic abnormalities. …
NAID 130001872381

The evidence of polymorphisms of the liver X receptor gene as a DNA-based biomarker for susceptibility to coronary artery disease in a Japanese population

Fukae Atsuki.et.al.
Acta Medica Nagasakiensia 55(2), 69-76, 2011-03
… Coronary artery disease (CAD) is a multifactorial and polygenic disorder, which arises due to atherosclerosis of the coronary arteries. …
NAID 110008455090

Examination of Adhesion Molecules, Homocysteine and hs-CRP in Patients with Polygenic Hypercholesterolemia and Isolated Hypertriglyceridemia

Calan Mehmet,Calan Ozlem,Gonen Mustafa Sait,Bilgir Ferda,Kebapcilar Levent,Kulac Esin,Cinali Turker,Bilgir Oktay
Internal Medicine 50(15), 1529-1535, 2011
… The present study aims to compare the levels of homocysteine, hs-CRP, E-selectin, sP-selectin, VCAM-1, ICAM-1 in patients with isolated hypertriglyceridemia and polygenic hypercholesterolemia. … Methods The following three groups were formed: polygenic hypercholesterolemia group (n=30), isolated hypertriglyceridemia group (n=30) and control group (n=30). …
NAID 130000969344

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★リンクテーブル★

リンク元	「多因子」「multifactorial」「多遺伝子」「ポリジーン」「multifactor」
拡張検索	「polygenic disease」「polygenic inheritance」