Gene family
A gene family is a set of several similar genes. They occur by the duplication of a single original gene. Usually they have similar biochemical functions. The idea that genes get duplicated is almost as old as the science of genetics.[1]
One such family are the genes for human haemoglobin subunits. The ten genes are in two clusters on different chromosomes, called the α-globin and β-globin loci. These two gene clusters are thought to have arisen from a precursor gene being duplicated, about 500 million years ago.[2]
The biggest gene family is said to be the olfaction genes.[3] The homeobox genes are another important group.[4]
Genes for the immune system include several gene families. They code for the major histocompatibility complex,[5] and the immunoglobulins.[6] The toll-like receptors are the main sensors of infection in mammals.[7][8]
Gene Family Media
Phylogenetic tree of the Mup gene family
Gene phylogeny as lines within grey species phylogeny. Top: An ancestral gene duplication produces two paralogs (histone H1.1 and 1.2).
References
- ↑ Taylor, John S. & Raes, Jeroen 2004. Duplication and divergence: the evolution of new genes and old ideas. Annual Review of Genetics 38: 615-643. [1] Archived 2016-05-25 at the Wayback Machine
- ↑ Nussbaum, Robert L.; McInnes, Roderick R.; Willard, Huntington F. (2016). Thompson & Thompson Genetics in Medicine (8th ed.). Philadelphia, PA: Elsevier. p. 25. ISBN 978-1-4377-0696-3.
- ↑ Niimura Y. & Nei M. 2003. Evolution of olfactory receptor genes in the human genome. Proceedings of the National Academy of Sciences of the United States of America 100 (21): 12235–40. [2] Archived 2017-03-15 at the Wayback Machine
- ↑ Bürglin T.R. Affolter M. 2015. Homeodomain proteins: an update. Chromosoma, 1–25. [3]
- ↑ Janeway CA Jr, Travers P, Walport M, et al. 2001. Immunobiology: The Immune System in health and disease. 5th edition. New York: Garland Science. The major histocompatibility complex and its functions. [4]
- ↑ Barclay A 2003. Membrane proteins with immunoglobulin-like domains--a master superfamily of interaction molecules. Seminars in Immunology 15 (4): 215–23. [5]
- ↑ Hoshino K. et al 1999. (1999). "Cutting edge: toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product". Journal of Immunology. 162 (7): 3749–52. doi:10.4049/jimmunol.162.7.3749. PMID 10201887. S2CID 7419784.
- ↑ Poltorak, Alexander 1998.; et al. (1998). "Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene". Science. 282 (5396): 2085–2088. doi:10.1126/science.282.5396.2085. PMID 9851930.