Day 30 (2pter-2p25.1): allantoicase, a protein that lost its function

"Alfred Baring Garrod, the gout specialist, discovers uric ac Wellcome V0011872" by http://wellcomeimages.org/indexplus/obf_images/7b/c5/cfbaf807df20f23e9ce2492aaa84.jpgGallery: http://wellcomeimages.org/indexplus/image/V0011872.html. Licensed under CC BY 4.0 via Wikimedia Commons - https://commons.wikimedia.org/wiki/File:Alfred_Baring_Garrod,_the_gout_specialist,_discovers_uric_ac_Wellcome_V0011872.jpg#/media/File:Alfred_Baring_Garrod,_the_gout_specialist,_discovers_uric_ac_Wellcome_V0011872.jpg

“Alfred Baring Garrod, the gout specialist, discovers uric ac Wellcome V0011872” by http://wellcomeimages.org/indexplus/obf_images/7b/c5/cfbaf807df20f23e9ce2492aaa84.jpg

Day 30 marks the beginning of Chromosome 2. This is a fascinating chromosome because it is the only one found in humans but not our primate relatives: it resulted from the fusion of two ancestral chromosome.

Today has 23 protein-coding genes including ALLNencoding the enzyme allantoicase. In fish and amphibians, allantoicase breaks down uric acid. In land vertebrates, this function has been taken over by other enzymes; in humans, it is lost (we excrete uric acid in our urine.)

Usually when a gene loses its necessity during evolution, it becomes a pseudogene, inactivated by random mutations, living on only as a genetic fossil. (The GULO pseudogene is an example – it gave our ancestors the ability to synthesize vitamin C.) ALLN is not a pseudogene because it actually makes a protein product still, and for some reason it has not accumulated the early stop codons that would ordinarily doom a pseudogene to nonsense-mediated decay. It may have gained a secondary function unrelated to uric acid metabolism, or a quirk of being near especially important genes may have kept it relatively mutation-free through a process called background selection.

Click here to see your ALLN gene at the start of Chromosome 2.

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