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Published 18 August 2003. doi:10.1083/jcb.200303174
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© The Rockefeller University Press, 0021-9525/2003/8/623 $5.00
The Journal of Cell Biology, Volume 162, Number 4, 623-633


Article

Distinct roles of G{alpha}i and Gß13F subunits of the heterotrimeric G protein complex in the mediation of Drosophila neuroblast asymmetric divisions



Fengwei Yu1, Yu Cai1, Rachna Kaushik1, Xiaohang Yang1 and William Chia2

1 Institute of Molecular and Cell Biology, Singapore 117609
2 MRC Centre for Developmental Neurobiology, London SE1 1UL, UK

Address correspondence to William Chia, MRC Centre for Developmental Neurobiology, 4th Fl., New Hunts House, Guy's Campus, King's College London, London SE1 1UL, UK. Tel.: 44-207-8486544. Fax: 44-207-8486550. email: william.chia{at}kcl.ac.uk; or Xiaohang Yang, Institute of Molecular and Cell Biology, 30 Medical Dr., Singapore 117609. Tel.: 65-687-47848. Fax: 65-677-91117. email: mcbyangn{at}imcb.nus.edu.sg

The asymmetric division of Drosophila neuroblasts involves the basal localization of cell fate determinants and the generation of an asymmetric, apicobasally oriented mitotic spindle that leads to the formation of two daughter cells of unequal size. These features are thought to be controlled by an apically localized protein complex comprising of two signaling pathways: Bazooka/Drosophila atypical PKC/Inscuteable/DmPar6 and Partner of inscuteable (Pins)/G{alpha}i; in addition, Gß13F is also required. However, the role of G{alpha}i and the hierarchical relationship between the G protein subunits and apical components are not well defined. Here we describe the isolation of G{alpha}i mutants and show that G{alpha}i and Gß13F play distinct roles. G{alpha}i is required for Pins to localize to the cortex, and the effects of loss of G{alpha}i or pins are highly similar, supporting the idea that Pins/G{alpha}i act together to mediate various aspects of neuroblast asymmetric division. In contrast, Gß13F appears to regulate the asymmetric localization/stability of all apical components, and Gß13F loss of function exhibits phenotypes resembling those seen when both apical pathways have been compromised, suggesting that it acts upstream of the apical pathways. Importantly, our results have also revealed a novel aspect of apical complex function, that is, the two apical pathways act redundantly to suppress the formation of basal astral microtubules in neuroblasts.

Key Words: neuroblast; asymmetric division; astral microtubules; heterotrimeric G proteins; Drosophila


F. Yu's present address is Temasek Life Sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604.

Abbreviations used in this paper: baz, bazooka; CNN, centrosomin; DaPKC, Drosophila atypical PKC; insc, inscuteable; mira, miranda; NB, neuroblast; pins, partner of inscuteable; pon, partner of numb; pros, prospera; wt, wild type.


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