Dcas Is Required for importin-α3 Nuclear Export and Mechano-Sensory Organ Cell Fate Specification in Drosophila

• DOI: 10.1006/dbio.2002.0612
• Publication Date: 2002-09-16T15:45:48Z
• Authors: Hildegard Tekotte; Daniela Berdnik; Tibor Török; Michael Buszczak; Lynn M Jones; Lynn Cooley; Jürgen A Knoblich; Ilan Davis
• Keywords: alpha Karyopherins; 0301 basic medicine; Embryo, Nonmammalian; Active Transport, Cell Nucleus; Apoptosis; 03 medical and health sciences; peripheral nervous system; Cellular Apoptosis Susceptibility Protein; mechano-sensory bristle development; Morphogenesis; Animals; Drosophila Proteins; RNA, Messenger; Molecular Biology; In Situ Hybridization; Phylogeny; Cse1p; nucleocytoplasmic transport; DNA Helicases; CAS; importin alpha nuclear export; Gene Expression Regulation, Developmental; Sense Organs; 01.06. Biológiai tudományok; Cell Biology; 3. Good health; Drosophila melanogaster; Drosophila; dcas; Mechanoreceptors; Developmental Biology

We have studied the in vivo function and tissue specificity of Dcas, the Drosophila ortholog of CAS, the importin beta-like export receptor for importin alpha. While dcas mRNA is specifically expressed in the embryonic central nervous system, Dcas protein is maternally supplied to all embryonic cells and its nuclear/cytoplasmic distribution varies in different tissues and times in development. Unexpectedly, hypomorphic alleles of dcas show specific transformations in mechano-sensory organ cell identity, characteristic of mutations that increase Notch signaling. Dcas is essential for efficient importin-alpha3 nuclear export in mechano-sensory cells and the surrounding epidermal cells and is indirectly required for the import of one component of the Notch pathway, but not others tested. We interpret the specificity of the dcas phenotype as indicating that one or more Notch signaling components are particularly sensitive to a disruption in nuclear protein import. We propose that mutations in house keeping genes often cause specific developmental phenotypes, such as those observed in many human genetic disorders.