The GC kinase Fray and Mo25 regulate Drosophila asymmetric divisions.
The GC kinase Fray and Mo25 regulate Drosophila asymmetric divisions.
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DOI：
10.1016/j.bbrc.2007.11.128
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发表时间：
2008-02
影响因子：
3.1
通讯作者：
Yoshihiro Yamamoto;Y. Izumi;F. Matsuzaki
中科院分区：
文献类型：
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作者：
Yoshihiro Yamamoto;Y. Izumi;F. Matsuzaki
Dorabuila神经母细胞为不对称细胞分裂提供了一个很好的模型，其中细胞命运决定因子如米兰达定位于基底皮质并分离到一个子细胞。然而，这一进程的基本机制仍然难以捉摸。我们发现Mo25和GC激酶Fray在这种调节中起作用。mo25和fray突变体在米兰达定位中显示出不可区分的缺陷。另一方面，果蝇Mo25与肿瘤抑制激酶Lkb1在体内相互作用，如在哺乳动物中所示。Lkb1的过度表达，它积累在细胞皮质，大大重新定位Mo25和Fray从细胞质到皮质，导致相同的表型为mo25突变的神经母细胞。从Lkb1过表达引起的这种缺陷中恢复需要同时过表达Mo25和Fray。我们从这些结果表明，Mo25和Fray一起或在果蝇不对称过程中的相同途径中运作，并且它们的功能平衡Lkb1。
Dorosophila 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.