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The KetelD dominant female-sterile mutations and their ketelr revertant alleles identify the Ketel gene, which encodes the importin-β (karyopherin-β) homologue of Drosophila melanogaster. Embryogenesis does not commence in the KetelD eggs deposited by the KetelD/+ females due to failure of cleavage nuclei formation. When injected into wild-type cleavage embryos, cytoplasm of the KetelD eggs does not inhibit nuclear protein import but prevents cleavage nuclei formation following mitosis. The Ketel+ transgenes slightly reduce effects of the KetelD mutations. The paternally derived KetelD alleles act as recessive zygotic lethal mutations: the KetelD/- hemizygotes, like the ketelr/ketelr and the ketelr/- zygotes, perish during second larval instar. The Ketel maternal dowry supports their short life. The KetelD-related defects originate most likely following association of the KetelD-encoded mutant molecules with a maternally provided partner. As in the KetelD eggs, embryogenesis does not commence in eggs of germline chimeras with ketelr/- germline cells and normal soma, underlining the dominant-negative nature of the KetelD mutations. The ketelr homozygous clones are fully viable in the follicle epithelium in wings and tergites. The Ketel gene is not expressed in most larval tissues, as revealed by the expression pattern of a Ketel promoter-lacZ reporter gene.

The KetelD Dominant-Negative Mutations Identify Maternal Function of the Drosophila Importin-β Gene Required for Cleavage Nuclei Formation