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Yamamoto, Y., Izumi, Y., Matsuzaki, F. (2008). The GC kinase Fray and Mo25 regulate Drosophila asymmetric divisions.  Biochem. Biophys. Res. Commun. 366(1): 212--218.
FlyBase ID
FBrf0202392
Publication Type
Research paper
Abstract

Drosophila neuroblasts provide an excellent model for asymmetric cell divisions, where cell-fate determinants such as Miranda localize at the basal cortex and segregate to one daughter cell. Mechanisms underlying this process, however, remain elusive. We found that Mo25 and the GC kinase Fray act in this regulation. mo25 and fray mutants show an indistinguishable defect in Miranda localization. On the other hand, Drosophila Mo25 interacts with the tumor suppressor kinase Lkb1 in vivo, as have shown in mammals. Overexpression of Lkb1, which accumulates in the cell cortex, drastically relocalizes both Mo25 and Fray from the cytoplasm to the cortex, causing the same phenotype as mo25-mutant neuroblasts. Recovery from this defect caused by Lkb1 overexpression requires simultaneous overexpression of Mo25 and Fray. We suggest from those results that Mo25 and Fray operate together or in the same pathway in Drosophila asymmetric processes, and that their function counterbalances Lkb1.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Biochem. Biophys. Res. Commun.
    Title
    Biochemical and Biophysical Research Communications
    Publication Year
    1959-
    ISBN/ISSN
    0006-291X
    Data From Reference
    Genes (5)