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Mol Cell Biol, March 1998, p. 1553-1561, Vol. 18, No. 3
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

The Drosophila Gene for Antizyme Requires Ribosomal Frameshifting for Expression and Contains an Intronic Gene for snRNP Sm D3 on the Opposite Strand

Ivaylo P. Ivanov,¹ Karl Simin,¹ Anthea Letsou,¹ John F. Atkins,¹ and Raymond F. Gesteland^1,2,*

Department of Human Genetics¹ and Howard Hughes Medical Institute,² University of Utah, Salt Lake City, Utah 84112

Received 20 October 1997/Returned for modification 14 November 1997/Accepted 18 November 1997

Previously, a Drosophila melanogaster sequence with high homology to the sequence for mammalian antizyme (ornithine decarboxylase antizyme) was reported. The present study shows that homology of this coding sequence to its mammalian antizyme counterpart also extends to a 5' open reading frame (ORF) which encodes the amino-terminal part of antizyme and overlaps the +1 frame (ORF2) that encodes the carboxy-terminal three-quarters of the protein. Ribosomes shift frame from the 5' ORF to ORF2 with an efficiency regulated by polyamines. At least in mammals, this is part of an autoregulatory circuit. The shift site and 23 of 25 of the flanking nucleotides which are likely important for efficient frameshifting are identical to their mammalian homologs. In the reverse orientation, within one of the introns of the Drosophila antizyme gene, the gene for snRNP Sm D3 is located. Previously, it was shown that two closely linked P-element transposon insertions caused the gutfeeling phenotype of embryonic lethality and aberrant neuronal and muscle cell differentiation. The present work shows that defects in either snRNP Sm D3 or antizyme, or both, are likely causes of the phenotype.

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^* Corresponding author. Mailing address: Department of Human Genetics, The University of Utah, 15N, 2030 E, Room 6160, Salt Lake City, UT 84112-5330. Phone: (801) 581-5190. Fax: (801) 585-3910. E-mail: rayg{at}howard.genetics.utah.edu.

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