WordNet

tending to undergo or resulting from mutation; "a mutant gene"
an animal that has undergone mutation
(biology) an organism that has characteristics resulting from chromosomal alteration (同)mutation, variation, sport

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突然変異種(堤)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/11/07 20:36:47」(JST)

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Auxotrophy (Ancient Greek: αὐξάνω "to increase"; τροφή "nourishment") is the inability of an organism to synthesize a particular organic compound required for its growth (as defined by IUPAC). An auxotroph is an organism that displays this characteristic; auxotrophic is the corresponding adjective. Auxotrophy is the opposite of prototrophy, which is characterized by the ability to synthesize all the compounds needed for growth.

The method of replica plating implemented by Esther Lederberg included auxotrophs that were temperature-sensitive; that is, their ability to synthesize was temperature-dependent. (Auxotrophs are usually not temperature-dependent. They can also depend on other factors.) Multiple auxotrophs can also coexist at the same time, within the same organism.

In genetics, a strain is said to be auxotrophic if it carries a mutation that renders it unable to synthesize an essential compound. For example, a yeast mutant with an inactivated uracil synthesis pathway gene is a uracil auxotroph (e.g., if the yeast Orotidine 5'-phosphate decarboxylase gene is inactivated, the resultant strain is a uracil auxotroph). Such a strain is unable to synthesize uracil and will only be able to grow if uracil can be taken up from the environment. This is the opposite of a uracil prototroph, or in this case a wild-type strain, which can still grow in the absence of uracil. Auxotrophic genetic markers are often used in molecular genetics; they were famously used in Beadle and Tatum's Nobel prize-winning work on the one gene-one enzyme hypothesis.

Researchers have used strains of E. coli auxotrophic for specific amino acids to introduce non-natural amino acid analogues into proteins. For instance cells auxotrophic for the amino acid phenylalanine can be grown in media supplemented with an analogue such as para-azido phenylalanine.

Many living things, including humans, are auxotrophic for large classes of compounds required for growth and must obtain these compounds through diet (see vitamin, essential nutrient, essential amino acid, essential fatty acid).

The complex pattern of evolution of vitamin auxotrophy across the eukaryotic tree of life is intimately connected with the interdependence between organisms.^[1]

The Ames test uses auxotrophic properties of the bacterium Salmonella typhimurium to test whether a given chemical can cause mutations.

Footnotes

^ Helliwell, Katherine E. et al. (2013). Widespread decay of vitamin-related pathways: coincidence or consequence?. Trends in Genetics, Volume 29, Issue 8, 469-478

External links

"Regulation of endosomal clathrin and retromer-mediated endosome to Golgi retrograde transport by the J-domain protein RME-8" - The EMBO Journal
"Pleiotropic effects of purine auxotrophy inRhizobium meliloti on cell surface molecules" - Springerlink
"Auxotrophy and Organic Compounds in the Nutrition of Marine Phytoplankton"

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English Journal

Identification of novel secreted fatty acids that regulate nitrogen catabolite repression in fission yeast.

Sun X1,2, Hirai G3,4, Ueki M5, Hirota H6, Wang Q4, Hongo Y7, Nakamura T7, Hitora Y1, Takahashi H8, Sodeoka M3,4, Osada H5, Hamamoto M2, Yoshida M1,6, Yashiroda Y1,6.
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Exometabolomics Assisted Design and Validation of Synthetic Obligate Mutualism.

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Histidine biosynthesis plays a crucial role in metal homeostasis and virulence of Aspergillus fumigatus.

Dietl AM1, Amich J2, Leal S3, Beckmann N1, Binder U4, Beilhack A2, Pearlman E3, Haas H1.
Virulence.Virulence.2016 Feb 6:1-12. [Epub ahead of print]
Aspergillus fumigatus is the most prevalent airborne fungal pathogen causing invasive fungal infections in immunosuppressed individuals. The histidine biosynthetic pathway is found in bacteria, archaebacteria, lower eukaryotes, and plants, but is absent in mammals. Here we demonstrate that deletion
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