Abstract：
The conserved bazooka (baz/par3) gene acts as a key regulator of asymmetrical cell divisions across the animal kingdom. Associated Par3/Baz-Par6-aPKC protein complexes are also well known for their role in the establishment of apical/basal cell polarity in epithelial cells. Here we define a novel, positive function of Baz/Par3 in the Notch pathway. Using Drosophila wing and eye development, we demonstrate that Baz is required for Notch signaling activity and optimal transcriptional activation of Notch target genes. Baz appears to act independently of aPKC in these contexts, as knockdown of aPKC does not cause Notch loss-of-function phenotypes. Using transgenic Notch constructs, our data positions Baz activity downstream of activating Notch cleavage steps and upstream of Su(H)/CSL transcription factor complex activity on Notch target genes. We demonstrate a biochemical interaction between NICD and Baz, suggesting that Baz is required for NICD activity before NICD binds to Su(H). Taken together, our data define a novel role of the polarity protein Baz/Par3, as a positive and direct regulator of Notch signaling through its interaction with NICD.
摘要：
保守的火箭筒（baz/par3）基因是整个动物界不对称细胞分裂的关键调节剂。相关的Par3/Baz-Par6-aPKC蛋白复合物在上皮细胞顶端/基底细胞极性建立中的作用也是众所周知的。这里我们定义了一部小说,Baz/Par3在Notch通路中的正功能。利用果蝇翅膀和眼睛发育，我们证明Baz是Notch信号活性和Notch靶基因的最佳转录激活所必需的。在这些情况下，巴兹似乎独立于aPKC，因为aPKC的敲低不会引起Notch功能丧失表型。使用转基因Notch构建体，我们的数据将Baz活性定位在Notch靶基因上激活Notch裂解步骤的下游和Su（H）/CSL转录因子复合物活性的上游。我们证明NICD和Baz之间的生化相互作用，这表明在NICD与Su(H)结合之前，Baz是NICD活性所必需的。一起来看,我们的数据定义了极性蛋白Baz/Par3作为Notch信号通过其与NICD相互作用的正向和直接调节因子的新作用.
