Genetics, Vol. 177, 1595-1608, November 2007, Copyright © 2007
doi:10.1534/genetics.107.080168

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

Daniel K. Spangenberg and Gail L. Waring1

Department of Biological Sciences, Marquette University, Milwaukee, Wisconsin 53233

1 Corresponding author: Department of Biological Sciences, Marquette University, P.O. Box 1881, Milwaukee, WI 53201-1881.
E-mail: gail.waring{at}marquette.edu

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.