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Genetics, Vol. 161, 763-772, June 2002, Copyright © 2002

P Elements Inserted in the Vicinity of or Within the Drosophila snRNP SmD3 Gene Nested in the First Intron of the Ornithine Decarboxylase Antizyme Gene Affect Only the Expression of SmD3

Heide Schenkela, Susanne Hankea, Cécilia De Lorenzoa, Rolf Schmitta, and Bernard M. Mechlera
a Department of Developmental Genetics, Deutsches Krebsforschungszentrum, D-69120 Heidelberg, Germany

Corresponding author: Bernard M. Mechler, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany., dev.genetics{at}dkfz-heidelberg.de (E-mail)

Communicating editor: T. SCHÜPBACH

The Drosophila gene for snRNP SmD3 (SmD3) is contained in reverse orientation within the first intron of the Ornithine Decarboxylase Antizyme (AZ) gene. Previous studies show that two closely linked P elements cause the gutfeeling phenotype characterized by embryonic lethality and aberrant neuronal and muscle cell differentiation. However, the exact nature of the gene(s) affected in the gutfeeling phenotype remained unknown. This study shows that a series of P inserts located within the 5'-untranslated region (5'-UTR) of SmD3 or its promoter affects only the expression of SmD3. Our analysis reveals that the gutfeeling phenotype associated with P elements inserted in the 5'-UTR of SmD3 results from amorphic or strongly hypomorphic mutations. In contrast, P inserts in the SmD3 promoter region reduce the expression of SmD3 without abolishing it and produce larval lethality with overgrown imaginal discs, brain hemispheres, and hematopoietic organs. The lethality of these mutations could be rescued by an SmD3+ transgene. Finally, inactivation of AZ was obtained by complementing with SmD3+ the deficiency Df(2R)guflex47 that uncovers both SmD3 and AZ. Interestingly, AZ inactivation causes a new phenotype characterized by late larval lethality and atrophy of the brain, imaginal discs, hematopoietic organs, and salivary glands.




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