No abstract

Krüppel is a member of the 'gap' class of segmentation genes of Drosophila melanogaster, mutations of which cause contiguous groups of segments of the fruitfly embryo to fail to develop. In the case of Krüppel mutant embryos, thoracic and anterior abdominal segments are deleted. The molecular cloning of the Krüppel locus will lead to an understanding of the crucial role that gap genes seem to have in early embryonic development. It has already allowed the identification of a blastoderm-specific Krüppel transcript and the phenotypic rescue of mutant embryos by injected cloned DNA.

The Krüppel (Kr) locus is a member of the 'gap' class of segmentation genes of Drosophila melanogaster. Mutations at the Kr locus cause the deletion of contiguous segments from the embryonic body pattern. We have elucidated the spatial and temporal characteristics of Kr gene expression during early embryo development, the localization of cytoplasmic Kr+ activity and its spatial requirement for normal segmentation.

The demonstration that a specific messenger RNA can be functionally inactivated in vivo by hybridization to complementary polynucleotide sequences suggests a direct approach to the study of gene function in cells of higher organisms. The experiments described here were designed to inhibit, by complementary RNA sequences, a specific gene function affecting the fate of the Drosophila embryo. We used the SP6 vector in vitro transcription system to transcribe parts of the normally untranscribed (nonsense) strand of the Krüppel (Kr) gene into complementary Kr RNA (Kr antisense RNA). Wild-type Drosophila embryos, injected with this RNA, developed into phenocopies of Kr mutant embryos.