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Address correspondence to Fumio Matsuzaki, Laboratory for Cell Asymmetry, Center for Developmental Biology, RIKEN, 2-2-3 Minatojima-Minamimachi, Chuou-ku, Kobe 650-0047, Japan. Tel.: 81-78-306-3217. Fax: 81-78-306-3215. email: fumio{at}cdb.riken.go.jp
Drosophila melanogaster neuroblasts (NBs) undergo asymmetric divisions during which cell-fate determinants localize asymmetrically, mitotic spindles orient along the apicalbasal axis, and unequal-sized daughter cells appear. We identified here the first Drosophila mutant in the G
1 subunit of heterotrimeric G protein, which produces G
1 lacking its membrane anchor site and exhibits phenotypes identical to those of Gß13F, including abnormal spindle asymmetry and spindle orientation in NB divisions. This mutant fails to bind Gß13F to the membrane, indicating an essential role of cortical G
1Gß13F signaling in asymmetric divisions. In G
1 and Gß13F mutant NBs, PinsG
i, which normally localize in the apical cortex, no longer distribute asymmetrically. However, the other apical components, Bazookaatypical PKCPar6Inscuteable, still remain polarized and responsible for asymmetric Miranda localization, suggesting their dominant role in localizing cell-fate determinants. Further analysis of Gß
and other mutants indicates a predominant role of Partner of InscuteableG
i in spindle orientation. We thus suggest that the two apical signaling pathways have overlapping but different roles in asymmetric NB division.
Key Words: epithelium; cell polarity; heterotrimeric G protein; spindle orientation; Drosophila melanogaster
Abbreviations used in this paper: Baz, Bazooka; DaPKC, Drosophila atypical PKC; DmPar-6, Drosophila Par-6; GMC, ganglion mother cell; Insc, Inscuteable; NB, neuroblast; Pins, Partner of Inscuteable.
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