The Ketel(D) dominant-negative mutations identify maternal function of thedrosophila importin-beta gene required for cleavage nuclei formation

The Ketel(D) dominant female-sterile mutations and their ketel(r) revertant alleles identify the Ketel gene, which encodes the importin-beta (karyophe rin-beta) homologue of Drosophila melanogaster: Embryogenesis does not comm ence in the Ketel(D) eggs deposited by the Ketel(D)/+ females due to failur e of cleavage nuclei formation. When injected into wild-type cleavage embry os, cytoplasm of the Ketel(D) eggs does not inhibit nuclear protein import but prevents cleavage nuclei formation following mitosis. The Ketel(+) tran sgenes slightly reduce effects of the Ketel(D) mutations. The paternally de rived Ketel(D) alleles act as recessive zygotic lethal mutations: the Ketel (D)/- hemizygotes, like the ketel(r)/ketel(r) and the ketel(r)/- zygotes, p erish during second larval instar. The Ketel maternal dowry supports their short life. The Ketel(D)-related defects originate most likely following as sociation of the Ketel(D)-encoded mutant molecules with a maternally provid ed partner. As in the Ketel(D) eggs, embryogenesis does not commence in egg s of germline chimeras with ketel(r)/- germline cells and normal soma, unde r lining the dominant-negative nature of the Ketel(D) mutations. The ketel( r) homozygous clones are fully viable in the follicle epithelium in wings a nd tergites. The Ketel gene is not expressed in most larval tissues, as rev ealed by the expression pattern of a Ketel promoter-lacZ reporter gene.