Cell shape is regulated by cell adhesion and cytoskeletal and membrane dynamics. Cell shape, adhesion, and motility have a complex relationship and understanding them is important in understanding developmental patterning and embryogenesis. Here we show that the lipid kinase phosphatidylinositol 4-kinase III beta (PI4KIIIβ) regulates cell shape, migration, and focal adhesion (FA) number. PI4KIIIβ generates phosphatidylinositol 4-phosphate (PI4P) from phosphatidylinositol and is highly expressed in a subset of human breast cancers. PI4KIIIβ and the PI4P it generates regulate a variety of cellular functions, ranging from control of Golgi structure, fly fertility, and Akt signaling. Here, we show that loss of PI4KIIIβ expression decreases cell migration and alters cell shape in NIH3T3 fibroblasts. The changes are accompanied by an increase in the number of FA in cells lacking PI4KIIIβ. Furthermore, we find that PI4P-containing vesicles move to the migratory leading edge during migration and that some of these vesicles tether to and fuse with FA. Fusion is associated with FA disassembly. This suggests a novel regulatory role for PI4KIIIβ and PI4P in cell adhesion and cell shape maintenance.

中文翻译：

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磷脂酰肌醇4-激酶IIIβ调节细胞形状，迁移和粘着斑数目。

细胞形状受细胞粘附以及细胞骨架和膜动力学的调节。细胞的形状，粘附性和运动性具有复杂的关系，理解它们对于理解发育模式和胚胎发生很重要。在这里，我们显示脂质激酶磷脂酰肌醇4-激酶III beta（PI4KIIIβ）调节细胞的形状，迁移和黏着斑（FA）数。PI4KIIIβ从磷脂酰肌醇生成4-磷酸磷脂酰肌醇（PI4P），并在人类乳腺癌的一部分中高度表达。PI4KIIIβ及其产生的PI4P调节多种细胞功能，范围包括控制高尔基体结构，果蝇繁殖力和Akt信号传导。在这里，我们显示PI4KIIIβ表达的丧失会降低细胞迁移并改变NIH3T3成纤维细胞的细胞形状。这些变化伴随着缺乏PI4KIIIβ的细胞中FA数量的增加。此外，我们发现含PI4P的囊泡在迁移过程中移至迁徙的前沿，并且这些囊泡中的一些束缚于FA并与FA融合。融合与FA拆卸有关。这表明PI4KIIIβ和PI4P在细胞粘附和细胞形状维持中具有新的调节作用。