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Effect of Alterations of the ATG Translation Start Codon of the APRT Gene

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Purine and Pyrimidine Metabolism in Man VI

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 253A))

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Abstract

The aprt gene locus has distinct advantages as a model for analysis of mutations in eucaryotic cells in culture. It is, for a eucaryotic gene, quite small. The minimal upstream through downstream region needed for normal function of the CHO gene when transfected into a host has been determined by deletion mapping to be from about 90 nt upstream of the transcription initiation site (about 155 nt upstream of the translation initiation site) through the gene to somewhere between 246 and 430 nt downstream of the translation stop codon. The 3′ untranslated sequence must include the first polyadenylation signal and a signal at least 10 nt and less than 200 nt 3′ of the polyadenylation signal. Thus the functional gene, including introns and 5′ and 3′ signals is somewhere between 2560 and 2380 nt long 1.

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© 1989 Plenum Press, New York

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Hershey, H.V., Taylor, M.W. (1989). Effect of Alterations of the ATG Translation Start Codon of the APRT Gene. In: Mikanagi, K., Nishioka, K., Kelley, W.N. (eds) Purine and Pyrimidine Metabolism in Man VI. Advances in Experimental Medicine and Biology, vol 253A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5673-8_77

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  • DOI: https://doi.org/10.1007/978-1-4684-5673-8_77

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5675-2

  • Online ISBN: 978-1-4684-5673-8

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