Mutant dec-1 Transgene Induces Dominant Female Sterility in Drosophila melanogaster

• Published in: Genetics (Austin) 2007-11, Vol.177 (3), p.1595-1608
• Main Authors: Spangenberg, D.K, Waring, G.L
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; amino acid sequences; Animals; Animals, Genetically Modified; Base Sequence; complementary DNA; DNA Primers - genetics; dominance (genetics); Drosophila melanogaster; Drosophila melanogaster - genetics; Drosophila melanogaster - metabolism; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Egg Proteins - genetics; Egg Proteins - metabolism; Female; female fertility; Females; Fertility; fruit flies; genes; Genes, Dominant; Genes, Insect; Infertility, Female - genetics; insect proteins; Insects; Investigations; Molecular Sequence Data; mutants; Mutation; nucleotide sequences; ova; Ovum - metabolism; Proteins; Recombinant Proteins - genetics; Recombinant Proteins - metabolism; Sequence Deletion; Studies; transgenes; Transgenic animals
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1534/genetics.107.080168

The Drosophila dec-1 gene produces three proproteins required for female fertility and eggshell assembly. The three proproteins are distinguished by their C termini. Fc106, the most abundant proprotein, is cleaved within the vitelline membrane to three mature derivatives in a developmentally regulated manner. To define sequences within fc106 that are critical for its function, we created wild-type and mutant versions of an fc106 cDNA transgene. The functional consequences of the mutations were assessed in dec-14, a female-sterile splicing mutant that does not produce the fc106 isoform. The fertility of dec-14 females was restored by the introduction of either a wild-type transgene or a transgene bearing a C-terminal deletion that included fc106-specific sequences. Surprisingly, the removal of internal coding sequences created an aberrant DEC-1 proprotein that induced female sterility when introduced into wild-type flies. Dominant female sterility was not associated with larger deletions that included the fc106 N terminus, suggesting that abnormal juxtaposition of N- and C-terminal sequences in the aberrant proprotein interfered with endogenous DEC-1 proteins. Changes in the fractionation behavior of the endogenous fc106 C-terminal derivative, s60, and morphological changes in the endochorion in response to expression of the aberrant proprotein support this interpretation.