The Drosophila melanogaster Ketel gene was identified via the Ketel(D) domi
nant female sterile mutations and their ketel(r) revertant alleles that are
recessive zygotic lethals. The maternally acting Ketel(D) mutations inhibi
t cleavage nuclei formation. We cloned the Ketel gene on the basis of a com
mon breakpoint in 38E1.2-3 in four ketel(r) alleles. The Ketel(+) transgene
s rescue Ketel(r)-associated zygotic lethality and slightly reduce Ketel(D)
-associated dominant female sterility. Ketel is a single copy gene. It is t
ranscribed to a single 3.6-kb mRNA, predicted to encode the 97-kD Ketel pro
tein. The 884-amino-acid sequence of Ketel is 60% identical and 78% similar
to that of human importin-beta, the nuclear import receptor for proteins w
ith a classical NLS. Indeed, Ketel supports import of appropriately designe
d substrates into nuclei of digitonin-permeabilized HeLa cells. As shown by
a polyclonal anti-Ketel antibody, nurse cells synthesize and transfer Kete
l protein into the oocyte cytoplasm from stage 11 of oogenesis. Tn cleavage
embryos the Ketel protein is cytoplasmic. The Ketel gene appears to be ubi
quitously expressed in embryonic cells. Western blot analysis revealed that
the Ketel gene is not expressed in several larval cell types of late third
instar larvae.