Infinitesimal model

Normally distributed phenotypes, like traits or diseases, happen because of many genes of small effects. If there were only a few genes, the phenotype would not be normally distributed.

The infinitesimal model or polygenic model is a way of understanding how traits are passed from parents to children using genes. It is used a lot in the study of how genes work and in studying all the genes in our DNA. This idea was first shared by Ronald Fisher in 1918. He said that many small genes together can decide how a trait shows up in a person.^[1]

In Fisher's 1918 paper, he explained that if a trait is decided by many genes, then the trait will be normally distributed in people.^[2] But it doesn't mean everyone will show the trait in the same way. It depends on their parents' genes.^[3] This idea helped people understand how the rules of genes and the ways traits show up can work together.^[4]

This model says that when less important genes change, the way traits show does not change fast. Because each gene has a tiny role.^[5] Changes in a phenotype like a trait or disease happen when many genes change. This is different from changes in only a few genes or one gene. It helps us understand how traits work.^[6]^[7]

References

↑ Nelson, Ronald M.. A century after Fisher: time for a new paradigm in quantitative genetics. Trends in Genetics 29 (12) (December 2013). p. 669–676. doi:10.1016/j.tig.2013.09.006.
↑ Boyle, Evan A.. An Expanded View of Complex Traits: From Polygenic to Omnigenic. Cell 169 (7) (June 2017). p. 1177–1186. doi:10.1016/j.cell.2017.05.038.
↑ Barton, N.H.. The infinitesimal model: Definition, derivation, and implications. Theoretical Population Biology 118 (December 2017). p. 50–73. doi:10.1016/j.tpb.2017.06.001.
↑ Turelli, Michael. Commentary: Fisher's infinitesimal model: A story for the ages. Theoretical Population Biology 118 (December 2017). p. 46–49. doi:10.1016/j.tpb.2017.09.003.
↑ Hill, William G. Applications of Population Genetics to Animal Breeding, from Wright, Fisher and Lush to Genomic Prediction. Genetics 196 (1) (2014). p. 1–16. doi:10.1534/genetics.112.147850.
↑ Martinez, Victor. Analysis of response to 20 generations of selection for body composition in mice: fit to infinitesimal model assumptions. Genetics Selection Evolution 32 (1) (2000-01-15). p. 3–21. doi:10.1186/1297-9686-32-1-3.
↑ Orr, H. Allen. The evolutionary genetics of adaptation: a simulation study. Genetics Research 74 (3) (December 1999). p. 207–214. doi:10.1017/S0016672399004164.

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[1] Nelson, Ronald M.. A century after Fisher: time for a new paradigm in quantitative genetics. Trends in Genetics 29 (12) (December 2013). p. 669–676. doi:10.1016/j.tig.2013.09.006.

[2] Boyle, Evan A.. An Expanded View of Complex Traits: From Polygenic to Omnigenic. Cell 169 (7) (June 2017). p. 1177–1186. doi:10.1016/j.cell.2017.05.038.

[3] Barton, N.H.. The infinitesimal model: Definition, derivation, and implications. Theoretical Population Biology 118 (December 2017). p. 50–73. doi:10.1016/j.tpb.2017.06.001.

[4] Turelli, Michael. Commentary: Fisher's infinitesimal model: A story for the ages. Theoretical Population Biology 118 (December 2017). p. 46–49. doi:10.1016/j.tpb.2017.09.003.

[5] Hill, William G. Applications of Population Genetics to Animal Breeding, from Wright, Fisher and Lush to Genomic Prediction. Genetics 196 (1) (2014). p. 1–16. doi:10.1534/genetics.112.147850.

[6] Martinez, Victor. Analysis of response to 20 generations of selection for body composition in mice: fit to infinitesimal model assumptions. Genetics Selection Evolution 32 (1) (2000-01-15). p. 3–21. doi:10.1186/1297-9686-32-1-3.

[7] Orr, H. Allen. The evolutionary genetics of adaptation: a simulation study. Genetics Research 74 (3) (December 1999). p. 207–214. doi:10.1017/S0016672399004164.

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